TRAIL联合谷胱甘肽过氧化物酶模拟物治疗乳腺癌的实验研究
|
摘要
肿瘤坏死因子相关的凋亡诱导配体(TRAIL , tumor necrosis factor-related apoptosis-inducing ligand)是肿瘤坏死因子(TNF)超家族成员之一。研究表明,TRAIL与靶细胞表面的死亡受体结合能够特异性地诱导多种肿瘤,如白血病、乳腺癌、直肠癌、膀胱癌、黑色素瘤、恶性神经胶质瘤、肺癌、前列腺癌等细胞凋亡,而对正常细胞没有影响。其独特的生物学特点给肿瘤治疗带来了新的希望,被公认为最有前途的治疗肿瘤的蛋白。近来,TRAIL的临床应用出现瓶颈,因为多数肿瘤细胞产生了对TRAIL不同程度的耐受机制。研究者们提出设想,能否通过某种药物消除肿瘤细胞对TRAIL的耐受性,而对其介导的凋亡敏感。已经有大量实验表明,通过与其他药物的联合作用,可以显著的增强TRAIL杀伤肿瘤细胞的能力。
谷胱甘肽过氧化物酶(GPx)模拟物对肿瘤细胞的增殖具有抑制作用。在本论文中,我们以乳腺癌细胞为研究对象,详细探讨了两种GPx模拟物:双硒桥联环糊精(2-SeCD)及双碲桥联环糊精(2-TeCD)作为TRAIL的敏化试剂联合诱导细胞凋亡的效应和相关机制。
1.在细胞水平验证了2-SeCD可以作为TRAIL的敏化试剂
首先以体外培养的乳腺癌细胞株MDA-MB-468与T47D细胞为例进行研究。结果表明, TRAIL单独作用的时候不能够杀伤乳腺癌细胞,而2-SeCD与其联合作用时,可以显著改变细胞的耐受性,恢复凋亡信号传导蛋白Caspase级联信号的传导,增加TRAIL诱导细胞凋亡的能力。通过对凋亡通路的研究,我们发现,2-SeCD的敏化机制在于剂量依赖性的上调死亡受体death receptor 5 (DR5)的表达含量,并抑制转录因子NF-κB亚基p65的核转移。
2.建立裸鼠乳腺癌皮下移植瘤模型,论证2-SeCD做为TRAIL敏化药物的可行性
在体外实验的基础上,我们通过建立MDA-MB-468乳腺癌荷瘤裸鼠模型,验证了2-SeCD与TRAIL联合应用治疗乳腺癌的药学效应。结果表明,药物联用可以显著抑制裸鼠体内肿瘤生长,并提高荷瘤鼠的生存质量。免疫组织化学染色结果显示,药物联合治疗组中细胞增殖抗原标记物Proliferating Cell Nuclear Antigen (PCNA)及Ki-67的表达含量减少,同时细胞凋亡标记物Terminal deoxyribonucleotidyl transferase–mediated dUTP nick end labeling (TUNEL)的表达含量明显增多。最后,2-SeCD上调DR5蛋白表达和下调p65-NF-κB的表达同样在裸鼠荷瘤组织中得到证实。
3.在细胞水平验证低剂量的2-TeCD可以作为TRAIL的敏化试剂
低剂量的2-TeCD可以与TRAIL协同杀伤乳腺癌细胞,并且通过顺序添加的方式可以将2-TeCD敏化TRAIL的浓度降低到亚微摩尔的水平。通过Annexin V/PI双染实验,以及Caspase活性检测实验,我们进一步证明了TRAIL和2-TeCD联合抑瘤的效应是通过激活Caspase途径,诱导细胞凋亡而实现的。最后2-TeCD敏化TRAIL通路的机制在于剂量依赖性的上调死亡受体DR5蛋白表达,同时阻断NF-κB的活化通路。
本研究结果证明GPx模拟物可以作为TRAIL的敏化试剂而应用于临床治疗中。
Tumor necrosis factor(TNF)α–related apoptosis-inducing ligand(TRAIL)is a member of the TNF family of cytokines. It exerts cytotoxic effects on malignant cells without any harm to normal cells. To date,five members of the human TNF receptor(TNFR)superfamily have been identified that can bind TRAIL,including death receptors DR4(TRAIL-R1)and DR5(TRAIL-R2),decoy receptors DcR1(TRAIL-R3)and DcR2(TRAIL-R4),as well as soluble receptor osteoprotegerin(OPG). However,only death receptors contain cytoplasmic death domain that are required for transmitting a cytotoxic signal. Following TRAIL engagement with either DR4 or DR5,the ligated death receptors cluster and initiat the formation of the death-inducing signaling complex(DISC). The functional death-inducing signaling complex is minimally composed of death receptors,FADD and Caspase 8 or 10. Active Caspases 8 and 10 cleave and directly activate downstream effector Caspases(3,6,7),which could ultimately result in apoptosis. Meanwhile,TRAIL receptors signaling pathway also leads to the activation of the nuclear factor-κB(NF-κB),which operates as a negative regulator for DISC formation. The subunit of NF-κB could up-regulate anti-apoptotic genes,such as cellular c-FLIP and c-IAPs,which eventually thwart activation of Caspases.
As a promising therapy agent for treatment of malignancies,TRAIL has been shown to induce apoptosis against breast carcinoma. Unfortunately,the majority of cell lines are insensitive to TRAIL-induced apoptosis,and the mechanism of the resistance has been attributed to dysfunction of different steps in the apoptosis pathways,as well as elevation of survival signals. The combination therapy was therefore envisaged,basing on the recent evidences that pretreatment of tumor cells with a chemotherapeutic agent could sensitize them to TRAIL. However,the combinations should be taken very carefully due to the potential toxicity to normal tissues. In this respect,it will be important to find a safe and effective agent to overcome TRAIL resistance in breast cancer therapy.
Seleno-cyclodextrin(2-selenium-bridgedβ-cyclodextrin,2-SeCD),a synthetic seleno-organic compound with unique glutathione peroxidase(GPx)-like activity,has exhibited anti-oxidant,anti-inflammatory and anti-tumor properties with very low toxicity. It has been extensivelydemonstrated as a promising substitute for ebselen,a well known GPx mimic,with enhanced enzymatic activity and water solubility. 2-tellurium-bridgedβ-cyclodextrin(2-TeCD),another synthetic organotellurium compound,has exhibited anti-oxidant and anti-inflammatory activities in vitro. Furthermore,2-TeCD has been shown to exhibit anti-tumor effects on breast carcinoma through selective inhibiting of thioredoxin reductase(TrxR)which is overexpressed in tumor tissues. Considering the anti-tumor property of the two agents,we hypothesized that their combination with TRAIL could be a promising strategy in the treatment of refractory breast tumors.
1. 2-SeCD sensitizes resistant human breast cancer cells to TRAIL-induced cytotoxicity in vitro.
We examined MDA-MB-468 and T47D cells for TRAIL sensitivity using different concentrations of recombinant human soluble TRAIL and/or 2-SeCD. Cells did not exhibit growth arrest by TRAIL alone treatment,while significant decrease of cell viability was observed with a synergistic treatment of 2-SeCD and TRAIL. Using the accepted criterion that apoptotic cells are Annexin V–positive/Propidium iodide–negative,we found that more than 50 percents of cells were undergo apoptosis in both of the cancer cell lines,upon exposure to the combination of the two agents. This experiment suggests that the sensitization of TRAIL-induced cytotoxicity by 2-SeCD is associated with apoptosis.
We next analyzed the Caspase-8 cleavage,a proximal event in the TRAIL-induced Caspase cascade. TRAIL alone failed to induce detectable Caspase-8 and Caspase-3 processing when compared to control. In contrast,cleaved-Caspases was clearly detected in both of the cancer cells when treated with the combination treatment of 2-SeCD and TRAIL. The immunoblotting results were further substantiated by Caspase activity assay. Compared to agent-alone group,the combination group significantly increased Caspase-3 and Caspase-8 activity in both of the MDA-MB-468 and T47D cells to about 4~6 times.
The activation of the Caspase-8 in combined treatment suggests that 2-SeCD targets an early step in the TRAIL-induced apoptosis pathway; we therefore evaluated the effects of 2-SeCD on expression of TRAIL receptor DR4 and DR5. Using Western bolting,flow cytometric analysis,RT-PCR reactions , as well as iRNA techniques we extensively showed that 2-SeCD dose-dependently induced the expression of TRAIL receptors DR5,but not DR4 on both mRNA and protein levels. These data suggest that up-regulation of DR5 by 2-SeCD is essential for the ability of TRAIL to induce apoptosis in resistant breast cancer cells.
2-SeCD treatment also suppressed TRAIL-induced nuclear factor-κB(NF-κB)prosurvival pathways by preventing cytosolic IκBαdegradation,as well as p65 nuclear translocation. Since traditional selenium compounds were not reported to target NF-κB activity in sensitizing TRAIL-resistant cancers,we hypothesize their unique GPx -like activity would be an attractive explanation. Therefore,inhibition of NF-κB nuclear translocation by 2-SeCD also contributes to its sensitization of TRAIL-induced apoptosis in breast cancer cells.
2. 2-SeCD and TRAIL results in tumor growth inhibition and apoptosis in vivo.
Based on the above findings,we next sought to evaluate whether the effect of 2-SeCD alone and in combination with TRAIL could inhibit tumor growth in vivo. MDA-MB-468 cells were subcutaneous injected into the right axilla of the female Balb/c nu/nu mice. TRAIL was ineffective in inhibiting the tumor growth; however,the combination of 2-SeCD and TRAIL exhibited significant inhibitory effects compared with other treatment groups. Immunohistochemical examination of tumor tissues revealed that 2-SeCD alone inhibited cell proliferation [proliferating cell nuclear antigen(PCNA)and Ki-67 staining] and induced apoptosis(TUNEL staining)in xenograft tumors. On the contrary,TRAIL had no significant effects compared with control group. Importantly,the combination of 2-SeCD and TRAIL were more effective in inhibiting tumor cell proliferation and inducing apoptosis than single agent alone. Finally,xenograft sections from each of the treatment groups were immunostained with anti-p65 and anti-DR5 antibodies. Treatment of mice with a combination of 2-SeCD and TRAIL significantly showed more expression of DR5 and less expression of p65-NF-κB proteins than that of mice treated with vehicles or TRAIL.
For the first time,we present clear evidences that 2-SeCD,a GPx mimic,can overcome TRAIL resistance in vitro and in vivo; therefore this combination provides a powerful therapeutic option for human breast cancer treatment.
3. Low doses of 2-TeCD could sensitizes resistant human breast cancer cells to TRAIL induced cytotoxicity in vitro.
2-tellurium-bridgedβ-cyclodextrin(2-TeCD)shares the unique chemical characteristics with its selenium counterparts(2-SeCD),but with a much better GPx mimic activity. Despite the antioxidants properties,2-TeCD has been recently shown to exhibit anti-tumor effects on breast carcinoma with a very low concentration. However,the application of 2-TeCD should be taken very carefully due to potential toxic effects of tellurium on kidney,hepatic and nervous system. In this study,we reported that 2-TeCD,in a low dose,could convert the TRAIL resistant breast cancer cells to TRAIL sensitive. Importantly,by using a sequential treatment protocol,where cells were first treated with 2-TeCD for 24 hours followed by TRAIL treatment,we could reduce the doses of 2-TeCD for TRAIL-sensitization in the submicromolar range. Using the Annexin V/ propidium iodide staining and Caspase activity assay , we then reavealed that the sensitization of TRAIL-Induced cytotoxicity by 2-TeCD is associated with apoptosis. Finally,the mechanism of sensitization could also attribute to the fact that 2-TeCD dose-dependently induced the expression of TRAIL receptors DR5,as well as down-regulated the activity of NF-κB.
谷胱甘肽过氧化物酶(GPx)模拟物对肿瘤细胞的增殖具有抑制作用。在本论文中,我们以乳腺癌细胞为研究对象,详细探讨了两种GPx模拟物:双硒桥联环糊精(2-SeCD)及双碲桥联环糊精(2-TeCD)作为TRAIL的敏化试剂联合诱导细胞凋亡的效应和相关机制。
1.在细胞水平验证了2-SeCD可以作为TRAIL的敏化试剂
首先以体外培养的乳腺癌细胞株MDA-MB-468与T47D细胞为例进行研究。结果表明, TRAIL单独作用的时候不能够杀伤乳腺癌细胞,而2-SeCD与其联合作用时,可以显著改变细胞的耐受性,恢复凋亡信号传导蛋白Caspase级联信号的传导,增加TRAIL诱导细胞凋亡的能力。通过对凋亡通路的研究,我们发现,2-SeCD的敏化机制在于剂量依赖性的上调死亡受体death receptor 5 (DR5)的表达含量,并抑制转录因子NF-κB亚基p65的核转移。
2.建立裸鼠乳腺癌皮下移植瘤模型,论证2-SeCD做为TRAIL敏化药物的可行性
在体外实验的基础上,我们通过建立MDA-MB-468乳腺癌荷瘤裸鼠模型,验证了2-SeCD与TRAIL联合应用治疗乳腺癌的药学效应。结果表明,药物联用可以显著抑制裸鼠体内肿瘤生长,并提高荷瘤鼠的生存质量。免疫组织化学染色结果显示,药物联合治疗组中细胞增殖抗原标记物Proliferating Cell Nuclear Antigen (PCNA)及Ki-67的表达含量减少,同时细胞凋亡标记物Terminal deoxyribonucleotidyl transferase–mediated dUTP nick end labeling (TUNEL)的表达含量明显增多。最后,2-SeCD上调DR5蛋白表达和下调p65-NF-κB的表达同样在裸鼠荷瘤组织中得到证实。
3.在细胞水平验证低剂量的2-TeCD可以作为TRAIL的敏化试剂
低剂量的2-TeCD可以与TRAIL协同杀伤乳腺癌细胞,并且通过顺序添加的方式可以将2-TeCD敏化TRAIL的浓度降低到亚微摩尔的水平。通过Annexin V/PI双染实验,以及Caspase活性检测实验,我们进一步证明了TRAIL和2-TeCD联合抑瘤的效应是通过激活Caspase途径,诱导细胞凋亡而实现的。最后2-TeCD敏化TRAIL通路的机制在于剂量依赖性的上调死亡受体DR5蛋白表达,同时阻断NF-κB的活化通路。
本研究结果证明GPx模拟物可以作为TRAIL的敏化试剂而应用于临床治疗中。
Tumor necrosis factor(TNF)α–related apoptosis-inducing ligand(TRAIL)is a member of the TNF family of cytokines. It exerts cytotoxic effects on malignant cells without any harm to normal cells. To date,five members of the human TNF receptor(TNFR)superfamily have been identified that can bind TRAIL,including death receptors DR4(TRAIL-R1)and DR5(TRAIL-R2),decoy receptors DcR1(TRAIL-R3)and DcR2(TRAIL-R4),as well as soluble receptor osteoprotegerin(OPG). However,only death receptors contain cytoplasmic death domain that are required for transmitting a cytotoxic signal. Following TRAIL engagement with either DR4 or DR5,the ligated death receptors cluster and initiat the formation of the death-inducing signaling complex(DISC). The functional death-inducing signaling complex is minimally composed of death receptors,FADD and Caspase 8 or 10. Active Caspases 8 and 10 cleave and directly activate downstream effector Caspases(3,6,7),which could ultimately result in apoptosis. Meanwhile,TRAIL receptors signaling pathway also leads to the activation of the nuclear factor-κB(NF-κB),which operates as a negative regulator for DISC formation. The subunit of NF-κB could up-regulate anti-apoptotic genes,such as cellular c-FLIP and c-IAPs,which eventually thwart activation of Caspases.
As a promising therapy agent for treatment of malignancies,TRAIL has been shown to induce apoptosis against breast carcinoma. Unfortunately,the majority of cell lines are insensitive to TRAIL-induced apoptosis,and the mechanism of the resistance has been attributed to dysfunction of different steps in the apoptosis pathways,as well as elevation of survival signals. The combination therapy was therefore envisaged,basing on the recent evidences that pretreatment of tumor cells with a chemotherapeutic agent could sensitize them to TRAIL. However,the combinations should be taken very carefully due to the potential toxicity to normal tissues. In this respect,it will be important to find a safe and effective agent to overcome TRAIL resistance in breast cancer therapy.
Seleno-cyclodextrin(2-selenium-bridgedβ-cyclodextrin,2-SeCD),a synthetic seleno-organic compound with unique glutathione peroxidase(GPx)-like activity,has exhibited anti-oxidant,anti-inflammatory and anti-tumor properties with very low toxicity. It has been extensivelydemonstrated as a promising substitute for ebselen,a well known GPx mimic,with enhanced enzymatic activity and water solubility. 2-tellurium-bridgedβ-cyclodextrin(2-TeCD),another synthetic organotellurium compound,has exhibited anti-oxidant and anti-inflammatory activities in vitro. Furthermore,2-TeCD has been shown to exhibit anti-tumor effects on breast carcinoma through selective inhibiting of thioredoxin reductase(TrxR)which is overexpressed in tumor tissues. Considering the anti-tumor property of the two agents,we hypothesized that their combination with TRAIL could be a promising strategy in the treatment of refractory breast tumors.
1. 2-SeCD sensitizes resistant human breast cancer cells to TRAIL-induced cytotoxicity in vitro.
We examined MDA-MB-468 and T47D cells for TRAIL sensitivity using different concentrations of recombinant human soluble TRAIL and/or 2-SeCD. Cells did not exhibit growth arrest by TRAIL alone treatment,while significant decrease of cell viability was observed with a synergistic treatment of 2-SeCD and TRAIL. Using the accepted criterion that apoptotic cells are Annexin V–positive/Propidium iodide–negative,we found that more than 50 percents of cells were undergo apoptosis in both of the cancer cell lines,upon exposure to the combination of the two agents. This experiment suggests that the sensitization of TRAIL-induced cytotoxicity by 2-SeCD is associated with apoptosis.
We next analyzed the Caspase-8 cleavage,a proximal event in the TRAIL-induced Caspase cascade. TRAIL alone failed to induce detectable Caspase-8 and Caspase-3 processing when compared to control. In contrast,cleaved-Caspases was clearly detected in both of the cancer cells when treated with the combination treatment of 2-SeCD and TRAIL. The immunoblotting results were further substantiated by Caspase activity assay. Compared to agent-alone group,the combination group significantly increased Caspase-3 and Caspase-8 activity in both of the MDA-MB-468 and T47D cells to about 4~6 times.
The activation of the Caspase-8 in combined treatment suggests that 2-SeCD targets an early step in the TRAIL-induced apoptosis pathway; we therefore evaluated the effects of 2-SeCD on expression of TRAIL receptor DR4 and DR5. Using Western bolting,flow cytometric analysis,RT-PCR reactions , as well as iRNA techniques we extensively showed that 2-SeCD dose-dependently induced the expression of TRAIL receptors DR5,but not DR4 on both mRNA and protein levels. These data suggest that up-regulation of DR5 by 2-SeCD is essential for the ability of TRAIL to induce apoptosis in resistant breast cancer cells.
2-SeCD treatment also suppressed TRAIL-induced nuclear factor-κB(NF-κB)prosurvival pathways by preventing cytosolic IκBαdegradation,as well as p65 nuclear translocation. Since traditional selenium compounds were not reported to target NF-κB activity in sensitizing TRAIL-resistant cancers,we hypothesize their unique GPx -like activity would be an attractive explanation. Therefore,inhibition of NF-κB nuclear translocation by 2-SeCD also contributes to its sensitization of TRAIL-induced apoptosis in breast cancer cells.
2. 2-SeCD and TRAIL results in tumor growth inhibition and apoptosis in vivo.
Based on the above findings,we next sought to evaluate whether the effect of 2-SeCD alone and in combination with TRAIL could inhibit tumor growth in vivo. MDA-MB-468 cells were subcutaneous injected into the right axilla of the female Balb/c nu/nu mice. TRAIL was ineffective in inhibiting the tumor growth; however,the combination of 2-SeCD and TRAIL exhibited significant inhibitory effects compared with other treatment groups. Immunohistochemical examination of tumor tissues revealed that 2-SeCD alone inhibited cell proliferation [proliferating cell nuclear antigen(PCNA)and Ki-67 staining] and induced apoptosis(TUNEL staining)in xenograft tumors. On the contrary,TRAIL had no significant effects compared with control group. Importantly,the combination of 2-SeCD and TRAIL were more effective in inhibiting tumor cell proliferation and inducing apoptosis than single agent alone. Finally,xenograft sections from each of the treatment groups were immunostained with anti-p65 and anti-DR5 antibodies. Treatment of mice with a combination of 2-SeCD and TRAIL significantly showed more expression of DR5 and less expression of p65-NF-κB proteins than that of mice treated with vehicles or TRAIL.
For the first time,we present clear evidences that 2-SeCD,a GPx mimic,can overcome TRAIL resistance in vitro and in vivo; therefore this combination provides a powerful therapeutic option for human breast cancer treatment.
3. Low doses of 2-TeCD could sensitizes resistant human breast cancer cells to TRAIL induced cytotoxicity in vitro.
2-tellurium-bridgedβ-cyclodextrin(2-TeCD)shares the unique chemical characteristics with its selenium counterparts(2-SeCD),but with a much better GPx mimic activity. Despite the antioxidants properties,2-TeCD has been recently shown to exhibit anti-tumor effects on breast carcinoma with a very low concentration. However,the application of 2-TeCD should be taken very carefully due to potential toxic effects of tellurium on kidney,hepatic and nervous system. In this study,we reported that 2-TeCD,in a low dose,could convert the TRAIL resistant breast cancer cells to TRAIL sensitive. Importantly,by using a sequential treatment protocol,where cells were first treated with 2-TeCD for 24 hours followed by TRAIL treatment,we could reduce the doses of 2-TeCD for TRAIL-sensitization in the submicromolar range. Using the Annexin V/ propidium iodide staining and Caspase activity assay , we then reavealed that the sensitization of TRAIL-Induced cytotoxicity by 2-TeCD is associated with apoptosis. Finally,the mechanism of sensitization could also attribute to the fact that 2-TeCD dose-dependently induced the expression of TRAIL receptors DR5,as well as down-regulated the activity of NF-κB.
引文
[1] Pitti RM,Marsters SA,Ruppert S,et al. J Biol Chem,1996,22:12687-90.
[2] Kaufmann SH,Steensma DP. On the TRAIL of a new therapy for leukemia. Leukemia,2005,19:2195-202.
[3] Rahman M,Pumphrey JG,Lipkowitz S. The TRAIL to targeted therapy of breast cancer. Adv Cancer Res,2009,103:43-73.
[4] Qiao L,Wong BC. Targeting apoptosis as an approach for gastrointestinal cancer therapy. Drug Resist Updat,2009,12:55-64.
[5] Sheikh MS,Huang Y,Fernandez-Salas EA,et al. The antiapoptotic decoy receptor TRID/TRAIL-R3 is a p53-regulated DNA damage-inducible gene that is overexpressed in primary tumors of the gastrointestinal tract. Oncogene,1999,18:4153-9.
[6] Rosevear HM,Lightfoot AJ,et al. The role of neutrophils and TNF-related apoptosis-inducing ligand(TRAIL)in bacillus Calmette-Guérin(BCG)immunotherapy for urothelial carcinoma of the bladder. Cancer Metastasis Rev,2009,28:345-53.
[7] Hao C,Beguinot F,Condorelli G,et al. Induction and intracellular regulation of tumor necrosis factor-related apoptosis-inducing ligand(TRAIL)mediated apotosis in human malignant glioma cells. Cancer Res,2001,61:1162-70.
[8] Wu M,Das A,Tan Y,et al. Induction of apoptosis in glioma cell lines by TRAIL/Apo-2l. JNeurosci Res,2000,61:464-70.
[9] The potential of death receptor 4- and 5-directed therapies in the treatment of lung cancer. Clin Lung Cancer,2007,8:413-9
[10] Bucur O,Ray S,Bucur MC,Almasan A. APO2 ligand/tumor necrosis factor-related apoptosis- inducing ligand in prostate cancer therapy. Front Biosci,2006,11:1549-68.
[11] Shimada O,Wu X,Jin X,et al. Human agonistic antibody to tumor necrosis factor-related apoptosis-inducing ligand receptor 2 induces cytotoxicity and apoptosis in prostate cancer and bladder cancer cells. Urology,2007,69:395-401.
[12] Bretz JD,Rymaszewski M,Arscott PL,et al. TRAIL death pathway expression and induction in thyroid follicular cells. J Biol Chem,1999,274:23627-32.
[13] Ryu HS,Chang KH,Chang SJ,et al. Expression of TRAIL(TNF-related apoptosis-inducing ligand)receptors in cervical cancer. Int J Gynecol Cancer,2000,10:417-24.
[14] Herr I,Schemmer P,Büchler MW. On the TRAIL to therapeutic intervention in liver disease. Hepatology,2007,46:266-74.
[15] Pfizenmaier K,Wajant H,Grell M. Tumor necrosis factors in 1996. Cytokine Growth Factor,1996,7:271-7.
[16] Walczak H,Krammer PH. The CD95(APO-1/Fas)and the TRAIL(APO-2L)apoptosis systems. Exp Cell Res,2000,256:58-66.
[17] Wiley SR,Schooley K,Smolak PJ,et al. Identification and characterization of a new member of TNF family that induce apoptosis. Immunity,1995,3:673-682.
[18] Seol DW,Billiar TR. Cysteine 230 modulates tumor necrosis factor-relate apoptosis-inducing ligand activity. Cancer Res,2000,60:3152-4.
[19] Hymowitz SG,O'Connell MP,Ultsch MH,et al. A unique zinc-binding site revealed by a high-resolution X-ray structure of homotrimeric Apo2L/TRAIL. Biochemistry,2000 ,39:633-40.
[20] Cha SS,Song YL,Oh BH. Specificity of molecular recognition learned from the crystal structures of TRAIL and the TRAIL: sDR5 complex. Vitam Horm,2004,67:1-17.
[21] Pitti RM,Marsters SA,Ruppert S,et al. Induction of apoptosis by Apo-2 ligand,a new member of the tumor necrosis factor cytokine family. J Biol Chem,1996,271:12687-90.
[22] Griffith TS,Lynch DH. Trail: a molecule with multiple receptor and control mechanisms. Curr Opin Immunol,1998,10:559-563
[23] Pan G,O‘Rourke K,Chinnaiyan AM,et al. The receptor for the cytotoxic ligand TRAIL. Science,1997,276:111–3.
[24] MacFarlane M,Ahmad M,Srinivasula SM,et al. Identification and molecular cloning of twonovel receptors for the cytotoxic ligand TRAIL. J Biol Chem,1997,272:25417-20.
[25] Pan H,Rourke K,chinnaiyan AM,et al. The receptor for the cytotoxic ligand TRAIL. Science,1997,276:1111.
[26] Walczak H,Degli-Esposti MA,Johnson RS,et al. TRAIL-R2: a novel apoptosis-mediating receptor for TRAIL. EMBO J,1997,16:5386-97.
[27] Papenfuss K,Cordier SM,Walczak H. Death receptors as targets for anti-cancer therapy. J Cell Mol Med,2008,12:2566-85.
[28] Elrod HA,Sun SY. Modulation of death receptors by cancer therapeutic agents. Cancer Biol Ther,2008,7:163-73.
[29] Van der Sloot AM,Tur V,Szegezdi E,et al. Designed tumor necrosis factor-related apoptosis-inducing ligand variants initiating apoptosis exclusively via the DR5 receptor. Proc Natl Acad Sci U S A,2006,103:8634-9.
[30] Kelley RF,Totpal K,Lindstrom SH,et al. Receptor-selective mutants of apoptosis-inducing ligand 2/tumor necrosis factor-related apoptosis-inducing ligand reveal a greater contribution of death receptor(DR)5 than DR4 to apoptosis signaling. J Biol Chem,2005,280:2205-12.
[31] Degli-Esposti MA,Smolak PJ,Walczak H,et al. Cloning and characterization of TRAIL-R3,a novel member of the emerging TRAIL receptor family. J Exp Med,1997,186:1165–70.
[32] Merino D,Lalaoui N,Morizot A,et al. Differential inhibition of TRAIL-mediated DR5-DISC formation by decoy receptors 1 and 2. Mol Cell Biol,2006,26:7046–7055.
[33] Marsters SA,Sheridan JP,Pitti RM,et al. A novel receptor for Apo2L/TRAIL contains a truncated death domain. Curr Biol,1997,7:1003–6.
[34] Degli-Esposti MA,Dougall WC,Smolak PJ,et al. The novel receptor TRAIL-R4 induces NF-kB and protects against TRAIL-mediated apoptosis,yet retains an incomplete death domain. Immunity,1997,7:813–20
[35] Clancy L,Mruk K,Archer K,et al. Preligand assembly domain-mediated ligand-independent association between TRAIL receptor 4(TR4)and TR2 regulates TRAIL-induced apoptosis. Proc Natl Acad Sci,2005,102:18099–104.
[36] Zhang XD,Franco AV,Nguyen T,et al. Differential localization and regulation of death and decoy receptors for TNF-relatedapoptosis-inducing ligand(TRAIL)in human melanoma cells. J Immunol,2000,164:3961-70.
[37] Emery JG,McDonnell P,Burke MB,et al. Osteoprotegerin is a receptor for the cytotoxic ligand TRAIL. J Biol Chem,1998,273:14363–7.
[38] Hofbauer LC. Osteoprotegerin ligand and osteoprotegerin: novel implications for osteoclast biology and bone metabolism. Eur J Endocrinol,1999,141:195-210.
[39] Lacey DL,Timms E,Tan HL,et al. Osteoprotegerin ligand is a cytokine that regulates osteoclast differentiation and activation. Cell,1998,93:165–76.
[40] Boatright KM,Renatus M,Scott FL,et al. A unified model for apical Caspase activation. Mol Cell,2003,11:529–41.
[41] Kischkel FC,Lawrence DA,Chuntharapai A. Apo2L/TRAIL-dependent recruitment of endogenous FADD and Caspase-8 to death receptors 4 and5. Immunity,2000,12:611-20.
[42] Kischkel FC,Hellbardt S,Behrmann I,et al. Cytotoxicity-dependent APO-1(Fas/CD95)- associated proteins form a death-inducing signaling complex(DISC)with the receptor. EMBO J,1995,14:5579-88.
[43] Bodmer JL,Holler N,Reynard S. TRAIL receptor-2 signals apoptosis through FADD and Caspase-8. Nat Cell Biol,2000,2:241-3.
[44] Chen Q,Ray S,Hussein MA,et al. Role of Apo2L/TRAIL and Bcl-2-family proteins in apoptosis of multiple myeloma. Leuk Lymphoma,2003,44:1209-14.
[45] Jiang X,Wang X. Cytochrome c promotes Caspase-9 activation by inducing nucleotide binding to Apaf-1. J Biol Chem,2000,275:31199-203.
[46] Du C,Fang M,Li Y,et al. Smac,a mitochondrial protein that promotes cytochrome c-dependent Caspase activation by eliminating IAP inhibition. Cell,2000,102:33-42.
[47] El-Deiry WS. Insights into cancer therapeutic design based on p53 and TRAIL receptor signaling. Cell Death Differ,2001,8:1066-75.
[48] Kim YS,Schwabe RF,Qian T,et al. TRAIL-mediated apoptosis requires NF-kappaB inhibition and the mitochondrial permeability transition in human hepatoma cells. Hepatology,2002,36:1498-508.
[49] Chen X,Kandasamy K,Srivastava RK. Differential roles of RelA(p65)and c-Rel subunits of nuclear factor kappa B in tumor necrosis factor-related apoptosis-inducing ligand signaling. Cancer Res,2003,63:1059-66.
[50] Crook NE,Clem RJ,Miller LK. An apoptosis-inhibiting baculovirus gene with a zinc finger-like motif. J Virol, 1993,67:2168-74.
[51] Deveraux QL,Takahashi R,Salvesen GS,et al. Xlinked IAP is a direct inhibitor of cell - death proteases. Nature 1997,388:300-4.
[52] Duckett CS,Nava VE,Gedrich RW,et al. A conserved family of cellular genes related to the baculovirus iap gene and encoding apoptosis inhibitors. EMBO J,1996,15:2685-94.
[53] Ekert PG,Silke J,Vaux DL. Caspase inhibitors. Cell Death Differ,1999,6:1081-6.
[54] LaCasse EC,Baird S,Korneluk RG,et al. The inhibitors of apoptosis(IAPs)and their emerging role in cancer. Oncogene,1998,17:3247 -59.
[55] Rothe M,Pan MG,Henzel WJ,et al. The TNFR2–TRAF signaling complex contains twonovel proteins related to baculoviral inhibitor of apoptosis proteins. Cell,1995,83:1243–52
[56] Roy N,Deveraux QL,Takahashi R,et al. The c - IAP - 1 and c - IAP - 2 proteins are direct inhibitors of specific Caspases. EMBO J,1997,16:6914– 25.
[57] Verhagen AM,Ekert PG,Pakusch M,et al. Identification of DIABLO,a mammalian protein that promotes apoptosis by binding to and antagonizing IAP proteins. Cell,2000,102:43– 53.
[58] Liston P,Roy N,Tamai K,et al. Suppression of apoptosis in mammalian cells by NAIP and arelated family of IAP genes. Nature,1996,379:349– 53.
[59] Thome M,Schneider P,Hofmann K,et al. Viral FLICE-inhibitory proteins(FLIPs)prevent apoptosis induced by death receptors. Nature,1997,386:517-21.
[60] IrmLer M,Thome M,Hahne M,et al. Inhibition of death receptor signals by cellular FLIP. Nature,1997,388:190-5.
[61] Kim Y,Suh N,Sporn M,et al. An inducible pathway for degradation of FLIP protein sensitizes tumor cells to TRAIL-induced apoptosis. J Biol Chem,2002,277:22320-9.
[62] Thorburn A. Death receptor-induced cell killing. Cell Signal,2004,16:139-44.
[63] Safa AR,Day TW,Wu CH. Cellular FLICE-like inhibitory protein(c-FLIP): a novel target for cancer therapy. Curr Cancer Drug Targets,2008,8:37-46.
[64] Goke R,Goke A,Goke B,et al. Regulation of TRAIL-induced apoptosis by transcription factors. Cell Immunol,2000,201:77-82.
[65] Costanzo A,Guiet C,Vito P. c-E10 is a Caspase-recruiting domain-containing protein that interacts with components of death receptors signaling pathway and activates nuclear factor-kappaB. J Biol Chem,1999,274:20127-32.
[66] Jeremias I,Kupatt C,Baumann B,et al. Inhibition of nuclear factor kappaB activation attenuates apoptosis resistance in lymphoid cells. Blood,1998,91:4624-31.
[67] Lin Y,Devin A,Rodriguez Y,et al. Cleavage of the death domain kinase RIP by Caspase-8 prompts TNF-induced apoptosis. Genes Dev,1999,13:2514-26.
[68] Martinon F,Holler N,Richard C,et al. Activation of a pro-apoptotic amplification loop through inhibition of NF-kappaB-dependent survival signals by Caspase-mediated inactivation of RIP. FEBS Lett,2000,468:134-6.
[69] Harper N , Farrow SN , Kaptein A , et al. Modulation of tumor necrosis factor apoptosis-inducing ligand-induced NF-kappa B activation by inhibition of apical Caspases. J Biol Chem,2001,276:34743-52.
[70] Dai Y,Liu M,Tang W,Li Y,et al. A Smac-mimetic sensitizes prostate cancer cells to TRAIL-induced apoptosis via modulating both IAPs and NF-kappaB. BMC Cancer,2009,9:392.
[71] Festa M,Petrella A,Alfano S,et al. R-roscovitine sensitizes anaplastic thyroid carcinoma cells to TRAIL-induced apoptosis via regulation of IKK/NF-kappaB pathway. Int J Cancer,2009,124:2728-36.
[72] Lee TJ,Jang JH,Noh HJ,et al. Overexpression of Par-4 sensitizes TRAIL-induced apoptosis via inactivation of NF-kappaB and Akt signaling pathways in renal cancer cells. J Cell Biochem,2010,109:885-95.
[73] Benedict CA,Banks TA,Ware CF. Death and survival: viral regulation of TNF signaling pathways. Curr Opin Immunol,2003,15:59-65.
[74] Clarke P,Meintzer SM,Gibson S,et al. Reovirus-induced apoptosis is mediated by TRAIL. J Virol,2000,74:8135-9.
[75] Sedger LM,Shows DM,Blanton RA,et al. IFN-gamma mediates a novel antiviral activity through dynamic modulation of TRAIL and TRAIL receptor expression. J Immunol,1999,163:920-6.
[76] Simmen KA,Singh J,Luukkonen BG,et al. Global modulation of cellular transcription by human cytomegalovirus is initiated by viral glycoprotein B. Proc Natl Acad Sci U S A,2001,98:7140-5.
[77] Shisler J,Yang C,Walter B,et al. The adenovirus E3-10.4K/14.5K complex mediates loss of cell surface Fas(CD95)and resistance to Fas-induced apoptosis. J Virol,1997,71:8299-306.
[78] Benedict CA,Norris PS,Prigozy TI,et al. Three adenovirus E3 proteins cooperate to evade apoptosis by tumor necrosis factor-related apoptosis-inducing ligand receptor-1 and -2. J Biol Chem,2001,276:3270-8.
[79] Thome M,Tschopp J.Regulation of lymphocyte proliferation and death by FLIP. Nat Rev Immunol,2001,1:50-8.
[80] Skaletskaya A,Bartle LM,Chittenden T,et al. A cytomegalovirus-encoded inhibitor of apoptosis that suppresses Caspase-8 activation. Proc Natl Acad Sci U S A,2001,98:7829-34.
[81] Geleziunas R,Xu W,Takeda K,et al. HIV-1 Nef inhibits ASK1-dependent death signalling providing a potential mechanism for protecting the infected host cell. Nature,2001,410:834-8.
[82] Chang HY,Nishitoh H,Yang X,et al. Activation of apoptosis signal-regulating kinase 1(ASK1)by the adapter protein Daxx. Science,1998,281:1860-3.
[83] Adrain C,Martin SJ. The mitochondrial apoptosome: a killer unleashed by the cytochrome seas. Trends Biochem Sci,2001,26:390-7.
[84] Henderson S,Huen D,Rowe M,et al. Epstein-Barr virus-coded BHRF1 protein,a viral homologue of Bcl-2,protects human B cells from programmed cell death. Proc Natl Acad SciU S A,1993,90:8479-83.
[85] Sarid R,Sato T,Bohenzky RA,et al. Kaposi's sarcoma-associated herpesvirus encodes a functional bcl-2 homologue. Nat Med,1997,3:293-8.
[86] Chinnaiyan AM,Prasad U,Shankar S,et al. Combined effect of tumor necrosis factor-related apoptosis-inducing ligand and ionizing radiation in breast cancer therapy. Proc Natl Acad Sci,2000,97:1754-9.
[87] Gong B,Almasan A. Apo2 ligand/TNF-related apoptosis-inducing ligand and death receptor 5 mediate the apoptotic signaling induced by ionizing radiation in leukemic cells. Cancer Res,2000,60:5754-60.
[88] Hori T,Kondo T,Kanamori M,et al. Ionizing radiation enhances tumor necrosis factor-related apoptosis-inducing ligand(TRAIL)-induced apoptosis through up-regulations of death receptor 4(DR4)and death receptor 5(DR5)in human osteosarcoma cells. J Orthop Res,2009.
[89] Keane MM,Ettenberg SA,Nau MM,et al. Chemotherapy augments TRAIL-induced apoptosis in breast cell lines. Cancer Res,1999,59:734-41.
[90] Singh TR,Shankar S,Chen X,et al. Synergistic interactions of chemotherapeutic drugs and tumor necrosis factor-related apoptosis-inducing ligand/Apo-2 ligand on apoptosis and on regression of breast carcinoma in vivo. Cancer Res,2003,63:5390-400.
[91] Ganten TM,Haas TL,Sykora J,et al. Enhanced Caspase-8 recruitment to and activation at the DISC is critical for sensitisation of human hepatocellular carcinoma cells to TRAIL-induced apoptosis by chemotherapeutic drugs. Cell Death Differ,2004,11:S86-96.
[92] Kim KM,Song JJ,An JY,et al. Pretreatment of acetylsalicylic acid promotes tumor necrosis factor-related apoptosis-inducing ligand-induced apoptosis by down-regulating BCL-2 gene expression. J Biol Chem,2005,280:41047-56.
[93] Yoo J,Lee YJ. Aspirin enhances tumor necrosis factor-related apoptosis-inducing ligand-mediated apoptosis in hormone-refractory prostate cancer cells through survivin down-regulation. Mol Pharmacol,2007,72:1586-92.
[94] Lu M,Strohecker A,Chen F,et al. Aspirin sensitizes cancer cells to TRAIL-induced apoptosis by reducing survivin levels. Clin Cancer Res,2008,14:3168-76.
[95] Liu X,Yue P,Zhou Z,et al. Death receptor regulation and celecoxib-induced apoptosis in human lung cancer cells. J Natl Cancer Inst,2004,96:1769-80.
[96] Liu X,Yue P,Sch?nthal AH,et al. Cellular FLICE-inhibitory protein down-regulation contributes to celecoxib-induced apoptosis in human lung cancer cells. Cancer Res,2006,66:11115-9.
[97] He Q,Luo X,Jin W,et al. Celecoxib and a novel COX-2 inhibitor ON09310 upregulate deathreceptor 5 expression via GADD153/CHOP. Oncogene,2008,27:2656-60.
[98] Rushworth SA,Micheau O. Molecular crosstalk between TRAIL and natural antioxidants in the treatment of cancer. Br J Pharmacol,2009,157:1186-8.
[99] Sah NK,Munshi A,Kurland JF,et al. Translation inhibitors sensitize prostate cancer cells to apoptosis induced by tumor necrosis factor-related apoptosis-inducing ligand(TRAIL)by activating c-Jun N-terminal kinase. J Biol Chem,2003,278:20593-602.
[100] Deeb D,Xu YX,Jiang H,et al. Curcumin(diferuloyl-methane)enhances tumor necrosis factor-related apoptosis-inducing ligand-induced apoptosis in LNCaP prostate cancer cells. Mol Cancer Ther,2003,2:95-103.
[101] Deeb D,Jiang H,Gao X,et al. Curcumin sensitizes prostate cancer cells to tumor necrosis factor-related apoptosis-inducing ligand/Apo2L by inhibiting nuclear factor-kappaB through suppression of IkappaBalpha phosphorylation. Mol Cancer Ther,2004,3:803-12.
[102] Deeb DD,Jiang H,Gao X,et al. Chemosensitization of hormone-refractory prostate cancer cells by curcumin to TRAIL-induced apoptosis. J Exp Ther Oncol,2005,5:81-91.
[103] Gao X,Deeb D,Jiang H,et al. Curcumin differentially sensitizes malignant glioma cells to TRAIL/Apo2L-mediated apoptosis through activation of proCaspases and release of cytochrome c from mitochondria. J Exp Ther Oncol,2005,5:39-48
[104] Jung EM,Lim JH,Lee TJ,et al. Curcumin sensitizes tumor necrosis factor-related apoptosis-inducing ligand(TRAIL)-induced apoptosis through reactive oxygen species-mediated upregulation of death receptor 5(DR5). Carcinogenesis,2005,26:1905-13.
[105] Khanbolooki S,Nawrocki ST,Arumugam T,et al. Nuclear factor-kappaB maintains TRAIL resistance in human pancreatic cancer cells. Mol Cancer Ther,2006,5:2251-60.
[106] Jung EM,Park JW,Choi KS,et al. Curcumin sensitizes tumor necrosis factor-related apoptosis-inducing ligand(TRAIL)-mediated apoptosis through CHOP-independent DR5 upregulation. Carcinogenesis,2006,27:2008-17.
[107] Kim H,Kim EH,Eom YW,et al. Sulforaphane sensitizes tumor necrosis factor-related apoptosis-inducing ligand(TRAIL)-resistant hepatoma cells to TRAIL-induced apoptosis through reactive oxygen species-mediated up-regulation of DR5. Cancer Res,2006,66:1740-50.
[108] Kamat AM,Sethi G,Aggarwal BB. Curcumin potentiates the apoptotic effects of chemotherapeutic agents and cytokines through down-regulation of nuclear factor-kappaB and nuclear factor-kappaB-regulated gene products in IFN-alpha-sensitive and IFN-alpha-resistant human bladder cancer cells. Mol Cancer Ther,2007,6:1022-30.
[109] Deeb D,Jiang H,Gao X,et al. Curcumin [1,7-bis(4-hydroxy-3-methoxyphenyl)-1-6-heptadine-3,5-dione; C21H20O6] sensitizes human prostate cancer cells to tumornecrosis factor-related apoptosis-inducing ligand/Apo2L-induced apoptosis by suppressing nuclear factor-kappaB via inhibition of the prosurvival Akt signaling pathway. J Pharmacol Exp Ther,2007,321:616-25.
[110] Wahl H,Tan L,Griffith K,et al. Curcumin enhances Apo2L/TRAIL-induced apoptosis in chemoresistant ovarian cancer cells. Gynecol Oncol,2007,105:104-12.
[111] Srivastava RK,Chen Q,Siddiqui I,et al. Linkage of curcumin-induced cell cycle arrest and apoptosis by cyclin-dependent kinase inhibitor p21(/WAF1/CIP1). Cell Cycle,2007,6:2953-61
[112] Andrzejewski T,Deeb D,Gao X,et al. Therapeutic efficacy of curcumin/TRAIL combination regimen for hormone-refractory prostate cancer. Oncol Res,2008,17:257-67.
[113] Teiten MH,Gaascht F,Eifes S,et al. Chemopreventive potential of curcumin in prostate cancer.Genes Nutr,2009 Oct 6.
[114] Shankar S,Ganapathy S,Chen Q,et al. Curcumin sensitizes TRAIL-resistant xenografts: molecular mechanisms of apoptosis,metastasis and angiogenesis. Mol Cancer,2008,7:16.
[115] Kamat AM,Tharakan ST,Sung B,et al. Curcumin potentiates the antitumor effects of Bacillus Calmette-Guerin against bladder cancer through the downregulation of NF-kappaB and upregulation of TRAIL receptors. Cancer Res,2009,69:8958-66.
[116] Kim H,Kim EH,Eom YW,et al. Sulforaphane sensitizes tumor necrosis factor-related apoptosis-inducing ligand(TRAIL)-resistant hepatoma cells to TRAIL-induced apoptosis through reactive oxygen species-mediated up-regulation of DR5. Cancer Res,2006,66:1740-50.
[117] Shankar S,Ganapathy S,Srivastava RK. Sulforaphane enhances the therapeutic potential of TRAIL in prostate cancer orthotopic model through regulation of apoptosis,metastasis,and angiogenesis. Clin Cancer Res,2008,14:6855-66.
[118] Jin CY,Moon DO,Lee JD,et al. Sulforaphane sensitizes tumor necrosis factor-related apoptosis-inducing ligand-mediated apoptosis through downregulation of ERK and Akt in lung adenocarcinoma A549 cells. Carcinogenesis,2007,28:1058-66.
[119] Shankar S,Ganapathy S,Srivastava RK. Sulforaphane enhances the therapeutic potential of TRAIL in prostate cancer orthotopic model through regulation of apoptosis,metastasis,and angiogenesis. Clin Cancer Res,2008,14:6855-66.
[120] Kallifatidis G,Rausch V,Baumann B,et al. Sulforaphane targets pancreatic tumour-initiating cells by NF-kappaB-induced antiapoptotic signalling. Gut,2009,58:949-63.
[121] Jin CY,Moon DO,Lee JD,et al. Sulforaphane sensitizes tumor necrosis factor-related apoptosis-inducing ligand-mediated apoptosis through downregulation of ERK and Akt in lung adenocarcinoma A549 cells. Carcinogenesis,2007,28:1058-66.
[122] Matsui TA,Sowa Y,Yoshida T,et al. Sulforaphane enhances TRAIL-induced apoptosis through the induction of DR5 expression in human osteosarcoma cells. Carcinogenesis,2006,27:1768-77.
[123] Toppo S,FlohéL,Ursini F,et al. Catalytic mechanisms and specificities of glutathione peroxidases: variations of a basic scheme. Biochim Biophys Acta,2009,1790:1486-500.
[124] Brigelius-FlohéR,Kipp A. Glutathione peroxidases in different stages of carcinogenesis. Biochim Biophys Acta,2009,1790:1555-68.
[125] Steinbrenner H,Sies H. Protection against reactive oxygen species by selenoproteins. Biochim Biophys Acta,2009,1790:1478-85.
[126] Brigelius-FlohéR. Glutathione peroxidases and redox-regulated transcription factors. Biol Chem, 2006,387:1329-35.
[127] Bartel J,Bartz T,Wolf C,et al. Activity of the glutathione peroxidase-2. Differences in the selenium-dependent expression between colon and small intestine. Cancer Genomics Proteomics,2007,4:369-72.
[128] Ottaviano FG,Tang SS,Handy DE,et al. Regulation of the extracellular antioxidant selenoprotein plasma glutathione peroxidase(GPx-3)in mammalian cells. Mol Cell Biochem,2009,327:111-26.
[129] Ding WQ,Lind SE,Phospholipid hydroperoxide glutathione peroxidase plays a role in protecting cancer cells from docosahexaenoic acid-induced cytotoxicity. Mol Cancer Ther,2007,6:1467-74.
[130] Meseguer M,Martínez-Conejero JA,et al. The human sperm glutathione system: a key role in male fertility and successful cryopreservation. Drug Metab Lett,2007,1:121-6.
[131] Namura S,Nagata I,Takami S,et al. Ebselen reduces cytochrome c release from mitochondria and subsequent DNA fragmentation after transient focal cerebral ischemia in mice. Stroke,2001,32:1906-11.
[132] Kotamraju S,Konorev EA,Joseph J,et al. Doxorubicin-induced apoptosis in endothelial cells and cardiomyocytes is ameliorated by nitrone spin traps and ebselen. Role of reactive oxygen and nitrogen species. J Biol Chem,2000,275:33585-92.
[133] Tanaka M,Takezawa N,Kumai T,et al. Ebselen protects against the reduction in levels of drug-metabolizing enzymes in livers of rats with deoxycholic acid-induced liver injury. Pharmacol Toxicol,2002,91:64-70.
[134] Wasser S,Lim GY,Ong CN,et al. Anti-oxidant ebselen causes the resolution of experimentally induced hepatic fibrosis in rats. J Gastroenterol Hepatol,2001,16:1244-53.
[135] Wu Q,Huang K. Effect of selenium compounds on the damage induced by oxysterol on ratarterial walls. Biol Trace Elem Res,2006,112:273-82.
[136] Engman L,Cotgreave I,Angulo M,et al. Diaryl chalcogenides as selective inhibitors of thioredoxin reductase and potential antitumor agents. Anticancer Res,1997,17:4599-605.
[137] Yang CF,Shen HM,Ong CN. Ebselen induces apoptosis in HepG(2)cells through rapid depletion of intracellular thiols. Arch Biochem Biophys,2000,374:142-52.
[138] Sharma V,Tewari R,Sk UH,et al. Ebselen sensitizes glioblastoma cells to Tumor Necrosis Factor(TNFalpha)-induced apoptosis through two distinct pathways involving NF-kappaB downregulation and Fas-mediated formation of death inducing signaling complex. Int J Cancer,2008,123:2204-12
[139] Sun Y,Mu Y,Ma S ,et al. The molecular mechanism of protecting cells against oxidative stress by 2-selenium-bridged beta-cyclodextrin with glutathione peroxidase activity. Biochim Biophys Acta,2005,1743:199-204.
[140] Jia ZD,Mu Y,Yan GL,et al. Comparison between the effects of 2-selenium-bridged beta-cyclodextrin and ebselen on treating SHRsp stroke. Chem Res Chinese U,2008,24:1–8.
[141] Lin TT,Wang BM,Li XY,et al. An insight into the protection of rat liver against ischemia/reperfusion injury by 2-selenium-bridged beta-cyclodextrin. Hepatol Res,2009,39:1125-36
[142] Wang BM(王冰梅). Studies on the Anti-tumor Effects of the two GPX Mimics and their action Mechanisms,PhD Thesis,Jilin University,2007.
[143] Wang K,Gong P,Liu L,et al. Effect of 2-TeCD on the expression of adhesion molecules in human umbilical vein endothelial cells under the stimulation of tumor necrosis factor-alpha. Int Immunopharmacol,2009,9:1087-91.
[144] McNaughton M,Engman L,Birmingham A,et al. Cyclodextrin-derived diorganyl tellurides as glutathione peroxidase mimics and inhibitors of thioredoxin reductase and cancer cell growth. J Med Chem,2004,47:233-9.
[1] Sies H. Ebselen,a selenoorganic compound as glutathione peroxidase mimic. Free Radic Biol Med,1993,14:313-23.
[2] Moussaoui S,Obinu MC,Daniel N,et al. The antioxidant ebselen prevents neurotoxicity and clinical symptoms in a primate model of Parkinson's disease. Exp Neurol,2000,166:235-45.
[3] Konz KH,Tiegs G,Wendel A. Protection by ebselen against endotoxin shock in rats or mice sensitized by galactosamine. Prog Clin Biol Res,1987,236A:281-8.
[4] Namura S,Nagata I,Takami S,et al. Ebselen reduces cytochrome c release from mitochondria and subsequent DNA fragmentation after transient focal cerebral ischemia in mice. Stroke, 2001,32:1906-11.
[5] Cotgreave IA,Johansson U,Westergren G,et al. The anti-inflammatory activity of ebselen but not thiols in experimental alveolitis and bronchiolitis. Agents Actions,1988,24:313-9.
[6] Gao JX,Issekutz AC. The effect of ebselen on polymorphonuclear leukocyte and lymphocyte migration to inflammatory reactions in rats. Immunopharmacology,1993,25:239-51.
[7] MJ Parnham,S Leyck,P Kuhl,J,et al. Ebselen:a new approach to the inhibition of peroxide-dependent inflammation. Int J Tissue React,1987,9:45-50.
[8] Yamaguchi T. Phase III trial of Ebselen. The American Stroke Association 28th International Stroke Conference,Phoenix,Arizona,2003. p. CTP20.
[9] Yang CF,Shen HM,Ong CN. Ebselen induces apoptosis in HepG(2)cells through rapid depletion of intracellular thiols. Arch Biochem Biophys,2000,374:142-52.
[10] Sharma V,Tewari R,Sk UH,et al. Ebselen sensitizes glioblastoma cells to Tumor NecrosisFactor(TNFalpha)-induced apoptosis through two distinct pathways involving NF-kappaB downregulation and Fas-mediated formation of death inducing signaling complex. Int J Cancer,2008,123:2204-12
[11] Suzuki K.Anti-oxidants for therapeutic use: why are only a few drugs in clinical use?Adv Drug Deliv Rev,2009,61:287-9.
[12] Sun Y,Mu Y,Ma S,et al. The molecular mechanism of protecting cells against oxidative stress by 2-selenium-bridged beta-cyclodextrin with glutathione peroxidase activity. Biochim Biophys Acta,2005,1743:199-204.
[13] Lin TT,Wang BM,Li XY,et al. An insight into the protection of rat liver against ischemia/reperfusion injury by 2-selenium-bridged beta-cyclodextrin. Hepatol Res,2009,39:1125-36
[14] Jia ZD,Mu Y,Yan GL, et al. Comparison between the effects of 2-selenium-bridged beta-cyclodextrin and ebselen on treating SHRsp stroke. Chem Res Chinese U,2008,24:1–8.
[15] Wang BM.(王冰梅)Studies on the Anti-tumor Effects of the two GPX Mimics and their action Mechanisms,PhD Thesis,Jilin University,2007.
[16] Wang K,Gong P,Liu L,et al. Effect of 2-TeCD on the expression of adhesion molecules in human umbilical vein endothelial cells under the stimulation of tumor necrosis factor-alpha. Int Immunopharmacol,2009,9:1087-91.
[17] McNaughton M,Engman L,Birmingham A,et al. Cyclodextrin-derived diorganyl tellurides as glutathione peroxidase mimics and inhibitors of thioredoxin reductase and cancer cell growth. J Med Chem,2004,47:233-9.
[18] Keane MM,Ettenberg SA,Nau MM,et al. Chemotherapy augments TRAIL-induced apoptosis in breast cell lines. Cancer Res,1999,59:734-41.
[19] Singh TR,Shankar S,Chen X,et al. Synergistic interactions of chemotherapeutic drugs and tumor necrosis factor-related apoptosis-inducing ligand/Apo-2 ligand on apoptosis and on regression of breast carcinoma in vivo. Cancer Res,2003,63:5390-400.
[20] Yamaguchi K,Uzzo RG,Pimkina J,et al. Methylseleninic acid sensitizes prostate cancer cells to TRAIL-mediated apoptosis. Oncogene,2005,24:5868-77.
[21] Hu H,Jiang C,Schuster T,Li GX,et al. Inorganic selenium sensitizes prostate cancer cells to TRAIL-induced apoptosis through superoxide/p53/Bax-mediated activation of mitochondrial pathway. Mol Cancer Ther,2006,5:1873-82.
[22] Kretz-Remy C,Mehlen P,Mirault ME,et al. Inhibition of IkB-a phosphorylation and degradation and subsequent NF-kB activation by glutathione peroxidase overexpression. J Cell Biol,1996,133:1083–93.
[23] Rygaard J,Povlsen CO. Heterotransplantation of a human malignant tumour to "Nude" mice. Acta Pathol Microbiol Scand,1969,77:758-60.
[24] Rygaard J. Immunobiology of the mouse mutant "Nude". Preliminary investigations. Acta Pathol Microbiol Scand,1969,77:761-2.
[25] Meotti FC,Borges VC,Zeni G,et al. Potential renal and hepatic toxicity of diphenyl diselenide,diphenyl ditelluride and Ebselen for rats and mice. Toxicol Lett,2003,143:9-16.
[26] Widy-Tyszkiewicz E,Piechal A,Gajkowska B,et al. Tellurium-induced cognitive deficits in rats are related to neuropathological changes in the central nervous system. Toxicol Lett,2002,131:203-14.
[1] Degli-Esposti M. To die or not to die--the quest of the TRAIL receptors. J Leukoc Biol,1999,65:535-42.
[2] Kischkel FC,Hellbardt S,Behrmann I,et al. Cytotoxicity-dependent APO-1(Fas/CD95)- associated proteins form a death-inducing signaling complex(DISC)with the receptor. EMBO J,1995,14:5579-88.
[3] Kischkel FC,Lawrence DA,Chuntharapai A,et al. Apo2L/TRAIL-dependent recruitment of endogenous FADD and Caspase-8 to death receptors 4 and 5. Immunity,2000,12:611-20.
[4] Kim YS,Schwabe RF,Qian T,et al. TRAIL-mediated apoptosis requires NF-kappaB inhibition and the mitochondrial permeability transition in human hepatoma cells. Hepatology,2002,36:1498-508.
[5] Kreuz S,Siegmund D,Scheurich P,et al. NF-kappaB inducers upregulate cFLIP,a cycloheximide-sensitive inhibitor of death receptor signaling. Mol Cell Biol , 2001 ,21:3964-73.
[6] Rahman M,Pumphrey JG,Lipkowitz S. The TRAIL to targeted therapy of breast cancer. Adv Cancer Res,2009,103:43-73.
[7] Keane MM,Ettenberg SA,Nau MM,et al. Chemotherapy augments TRAIL-induced apoptosis in breast cell lines. Cancer Res,1999,59:734-41.
[8] Singh TR,Shankar S,Chen X,et al. Synergistic interactions of chemotherapeutic drugs and TRAIL /Apo-2 ligand on apoptosis and on regression of breast carcinoma in vivo. Cancer Res,2003,63:5390-400.
[9] Ganten TM,Koschny R,Sykora J,et al. Preclinical differentiation between apparently safe and potentially hepatotoxic applications of TRAIL either alone or in combination with chemotherapeutic drugs. Clin Cancer Res,2006,12:2640-6.
[10] Koschny R,Ganten TM,Sykora J,et al. TRAIL/bortezomib cotreatment is potentiallyhepatotoxic but induces cancer-specific apoptosis within a therapeutic window. Hepatology,2007,45:649-58.
[11] Jia ZD,Mu Y,Yan GL,et al. Comparison between the effects of 2-selenium-bridged beta-cyclodextrin and ebselen on treating SHRsp stroke. Chem Res Chinese U,2008,24:1–8.
[12] Liu J,Luo G,Ren X,et al. A bis-cyclodextrin diselenide with glutathione peroxidase-like activity. Biochim Biophys Acta,2000,1481:222-8.
[13] Sun Y,MuY,Ma S,et al. The molecular mechanism of protecting cells against oxidative stress by 2-selenium-bridged beta-cyclodextrin with glutathione peroxidase activity. Biochim Biophys Acta,2005,1743:199-204.
[14] Yamaguchi K,Uzzo RG,Pimkina J,et al. Methylseleninic acid sensitizes prostate cancer cells to TRAIL-mediated apoptosis. Oncogene,2005,24:5868-77.
[15] Hu H,Jiang C,Schuster T,Li GX,Daniel PT,LüJ. Inorganic selenium sensitizes prostate cancer cells to TRAIL-induced apoptosis through superoxide/p53/Bax-mediated activation of mitochondrial pathway. Mol Cancer Ther,2006,5:1873-82.
[16] Venkateswaran V,Klotz LH,Fleshner NE. Selenium modulation of cell proliferation and cell cycle biomarkers in human prostate carcinoma cell lines. Cancer Res,2002,62:2540-5.
[17] Madhunapantula SV,Desai D,Sharma A,Huh SJ,Amin S,Robertson GP. PBISe,a novel selenium-containing drug for the treatment of malignant melanoma. Mol Cancer Ther,2008,7:1297-308.
[18] Hyer ML,Croxton R,Krajewska M,et al. Synthetic triterpenoids cooperate with TRAIL to induce apoptosis of breast cancer cells. Cancer Res,2005,65:4799-808.
[19] Walczak H,Haas TL. Biochemical analysis of the native TRAIL death-inducing signaling complex. Methods Mol Biol,2008,414:221-39.
[20] Keane MM,Rubinstein Y,Cuello M,et al. Inhibition of NF-kappaB activity enhances TRAIL mediated apoptosis in breast cancer cell lines. Breast Cancer Res Treat,2000,64:211-9.
[21] Yamanaka T,Shiraki K,Sugimoto K,et al. Chemotherapeutic agents augment TRAIL-induced apoptosis in human hepatocellular carcinoma cell lines. Hepatology,2000,32:482-90.
[22] Yu R,Mandlekar S,Ruben S,Ni J,et al. TRAIL-mediated apoptosis in androgen-independent prostate cancer cells. Cancer Res,2000,60:2384-9.
[23] Yeh CC,Deng YT,Sha DY,et al. Suberoylanilide hydroxamic acid sensitizes human oral cancer cells to TRAIL-induced apoptosis through increase DR5 expression. Mol Cancer Ther,2009,8:2718-25.
[24] Zou W,Yue P,Khuri FR,et al. Coupling of endoplasmic reticulum stress to CDDO-Me induced up-regulation of death receptor 5 via a CHOP-dependent mechanism involving JNKactivation. Cancer Res,2008,68:7484-92.
[25] Lu M,Xia L,Hua H,et al. Acetyl-keto-beta-boswellic acid induces apoptosis through a death receptor 5-mediated pathway in prostate cancer cells. Cancer Res,2008,68:1180-6.
[26] Son YG,Kim EH,Kim JY,et al. Silibinin sensitizes human glioma cells to TRAIL-mediated apoptosis via DR5 up-regulation and down-regulation of c-FLIP and survivin. Cancer Res,2007,67:8274-84.
[27] Ghosh S,Baltimore D. Activation in vitro of NF-kappa B by phosphorylation of its inhibitor I kappa B. Nature,1990,344:678-82.
[28] Beg AA,Ruben SM,Scheinman RI,et al. I kappa B interacts with the nuclear localization sequences of the subunits of NF-kappa B: a mechanism for cytoplasmic retention. Genes Dev,1992,6:1899-913.
[29] Oya M,Ohtsubo M,Takayanagi A,et al. Constitutive activation of nuclear factor-kappaB prevents TRAIL-induced apoptosis in renal cancer cells. Oncogene,2001,20:3888-96.
[30] Khanbolooki S,Nawrocki ST,Arumugam T,et al. Nuclear factor-kappaB maintains TRAIL resistance in human pancreatic cancer cells. Mol Cancer Ther,2006,5:2251-60.
[31] Li S,Yan T,Yang JQ,Oberley TD,et al. The role of cellular glutathione peroxidase redox regulation in the suppression of tumor cell growth by manganese superoxide dismutase. Cancer Res,2000,60:3927-39.
[32] Brar SS,Kennedy TP,Whorton AR,et al. Reactive oxygen species from NAD(P)H:quinone oxidoreductase constitutively activate NF-kappaB in malignant melanoma cells. Am J Physiol Cell Physiol,2001,280:C659-76.
[33] Kretz-Remy C,Mehlen P,Mirault ME,et al. Inhibition of IkB-a phosphorylation and degradation and subsequent NF-kB activation by glutathione peroxidase overexpression. J Cell Biol,1996,133:1083–93.
[34] Li Q,Sanlioglu S,Li S,et al. GPx-1 gene delivery modulates NFkappaB activation following diverse environmental injuries through a specific subunit of the IKK complex. Antioxid Redox Signal,2001,3:415-32.
[1] Rygaard J. Immunobiology of the mouse mutant "Nude". Preliminary investigations. Acta Pathol Microbiol Scand,1969,77:761-2.
[2] Giovanella BC. Experimental chemotherapy of human tumors heterotransplanted in nude mice. Antibiot Chemother,1980,28:21-7.
[3] Giovanella BC,Fogh J. The nude mouse in cancer research. Adv Cancer Res,1985,44:69-120.
[4] Dorsey JF,Mintz A,Tian X,et al. Tumor necrosis factor-related apoptosis-inducing ligand(TRAIL)and paclitaxel have cooperative in vivo effects against glioblastoma multiforme cells. Mol Cancer Ther, 2009,8:3285-95.
[5] Shankar S,Davis R,Singh KP,et al. Suberoylanilide hydroxamic acid(Zolinza/vorinostat)sensitizes TRAIL-resistant breast cancer cells orthotopically implanted in BALB/c nude mice.Mol Cancer Ther,2009,8:1596-605.
[6] Zhang X,Li W,Olumi AF. Low-dose 12-O-tetradecanoylphorbol-13-acetate enhances tumor necrosis factor related apoptosis-inducing ligand induced apoptosis in prostate cancer cells. Clin Cancer Res,2007,13:7181-90.
[7] Hyer ML,Croxton R,Krajewska M,et al. Synthetic triterpenoids cooperate with tumor necrosis factor-related apoptosis-inducing ligand to induce apoptosis of breast cancer cells. Cancer Res,2005,65:4799-808.
[8] Shankar S,Chen X,Srivastava RK. Effects of sequential treatments with chemotherapeutic drugs followed by TRAIL on prostate cancer in vitro and in vivo. Prostate,2005,62:165-86.
[9] Singh TR,Shankar S,Chen X,et al. Synergistic interactions of chemotherapeutic drugs and tumor necrosis factor-related apoptosis-inducing ligand/Apo-2 ligand on apoptosis and on regression of breast carcinoma in vivo. Cancer Res,2003,63:5390-400.
[10] Moldovan GL,Pfander B,Jentsch S. PCNA,the maestro of the replication fork. Cell,2007,129:665-79.
[11] Esteva FJ,Hortobagyi GN. Prognostic molecular markers in early breast cancer. Breast Cancer Res. Breast Cancer Res, 2004,6:109-18.
[12] Scholzen T,Gerdes J. The Ki-67 protein: from the known and the unknown. J Cell Physiol,2000,182:311-22.
[13] Allen RT,Hunter WJ 3rd,Agrawal DK. Morphological and biochemical characterization and analysis of apoptosis. J Pharmacol Toxicol Methods,1997,37:215-28.
[14] Walker RA. Immunohistochemical evaluation of tumours. Curr Opin Immunol,1989,1:878-82.
[1] W?hler F,Justus Liebigs. Ann. Chem. 1840,35: 111.
[2] Andersson CM,Brattsand R,Hallberg A,et al. Diaryl tellurides as inhibitors of lipid peroxidation in biological and chemical systems. Free Radic Res,1994,20:401-10.
[3] Engman L,Stern D,Frisell H ,et al. Synthesis,antioxidant properties,biological activity and molecular modelling of a series of chalcogen analogues of the 5-lipoxygenase inhibitor DuP 654. Bioorg Med Chem,1995,3:1255-62.
[4] Wieslander E,Engman L,Svensj? E,et al. Antioxidative properties of organotellurium compounds in cell systems. Biochem Pharmacol,1998,55:573-84.
[5] Tiano L,Fedeli D,Santroni AM,et al. Effect of three diaryl tellurides,and an organoselenium compound in trout erythrocytes exposed to oxidative stress in vitro. Mutat Res,2000,464:269-77.
[6] Engman L,Gupta V. Tetrahydrofuran Derivatives from Epoxides via Group Transfer Cyclization or Reductive Radical Cyclization of Organotellurium and Organoselenium Intermediates. J Org Chem,1997,62:157-173.
[7] Malmstr?m J , Jonsson M , Cotgreave IA , et al. The antioxidant profile of 2 ,3-dihydrobenzo[b]furan-5-ol and its 1-thio,1-seleno,and 1-telluro analogues. J Am Chem Soc, 2001,123:3434-40.
[8] Sredni B,Caspi RR,Lustig S,et al. The biological activity and immunotherapeutic properties of AS-101,a synthetic organotellurium compound. Nat Immun Cell Growth Regul,1988,7:163-8.
[9] Sredni B,Caspi RR,Klein A,et al. A new immunomodulating compound(AS-101)with potential therapeutic application. Nature,1987,330:173-6.
[10] Shani A,Tichler T,Catane R,et al. Immunologic effects of AS101 in the treatment of cancer patients. Nat Immun Cell Growth Regul,1990,9:182-90.
[11] Kalechman Y,Sotnik-Barkai I,Albeck M,et al. Protection of bone marrow stromal cells from the toxic effects of cyclophosphamide in vivo and of ASTA-Z 7557 and etoposide in vitro by ammonium trichloro(dioxyethylene-O-O')tellurate(AS101). Cancer Res,1993,53:1838-44.
[12] Kalechman Y,Gafter U,Barkai IS,et al. Mechanism of radioprotection conferred by the immunomodulator AS101. Exp Hematol,1993,21:150-5.
[13] Kalechman Y,Sotnik-Barkai I,Albeck M,et al. The effect of AS101 on the reconstitution of T-cell reactivity following irradiation or cyclophosphamide treatment. Exp Hematol,1992,20:1302-8.
[14] Kalechman Y,Albeck M,Sredni B. In vivo synergistic effect of the immunomodulator AS101 and the PKC inducer bryostatin. Cell Immunol,1992,143:143-53.
[15] Kalechman Y,Barkai IS,Albeck M,et al. Use and mechanism of action of AS101 in protecting bone marrow colony forming units-granulocyte-macrophage following purging with ASTA-Z 7557. Cancer Res,1991,51:5614-20.
[16] Kalechman Y,Albeck M,Oron M,et al. Protective and restorative role of AS101 in combination with chemotherapy. Cancer Res,1991,51:1499-503.
[17] Kalechman Y,Albeck M,Oron M,et al. Radioprotective effects of the immunomodulator AS101, J Immunol,1990,145:1512-7.
[18] Sredni B,Kalechman Y,Albeck M,et al. Cytokine secretion effected by synergism of theimmunomodulator AS101 and the protein kinase C inducer bryostatin. Immunology,1990,70:473-7.
[19] Kalechman Y,Shani A,Albeck M,et al. Induction of acute phase proteins in mice and humans by treatment with AS101 , an immunomodulator with radioprotective properties. Immunopharmacology,1995,29:149-58.
[20] Sailer BL,Liles N,Dickerson S,et al. Organotellurium compound toxicity in a promyelocytic cell line compared to non-tellurium-containing organic analog. Toxicol In Vitro,2004,18:475-82.
[21] Sailer BL,Liles N,Dickerson S,et al. Cytometric determination of novel organotellurium compound toxicity in a promyelocytic(HL-60)cell line. Arch Toxicol,2003,77:30-6.
[22] Urig S,Becker K. On the potential of thioredoxin reductase inhibitors for cancer therapy. Semin Cancer Biol,2006,16:452-65.
[23] Pennington JD,Jacobs KM,Sun L,et al. Thioredoxin and thioredoxin reductase as redox-sensitive molecular targets for cancer therapy. Curr Pharm Des,2007,13:3368-77.
[24] Engman L,Kandra T,Gallegos A,et al. Water-soluble organotellurium compounds inhibit thioredoxin reductase and the growth of human cancer cells. Anticancer Drug Des,2000,15:323-30.
[25] Engman L,Al-Maharik N,McNaughton M,et al. Thioredoxin reductase and cancer cell growth inhibition by organotellurium antioxidants. Anticancer Drugs,2003,14:153-61.
[26] Laden BP,Porter TD,et al. Inhibition of human squalene monooxygenase by tellurium compounds: evidence of interaction with vicinal sulfhydryls. J Lipid Res,2001,42:235-40
[27] Goodrum JF. Role of organotellurium species in tellurium neuropathy. Neurochem Res,1998,23:1313-9.
[28] Borges VC,Rocha JB,Nogueira CW. Effect of diphenyl diselenide,diphenyl ditelluride and ebselen on cerebral Na(+),K(+)-ATPase activity in rats. Toxicology,2005,215:191-7.
[29] Meotti FC,Borges VC,Zeni G,et al. Potential renal and hepatic toxicity of diphenyl diselenide,diphenyl ditelluride and Ebselen for rats and mice. Toxicol Lett,2003,143:9-16.
[30] Widy-Tyszkiewicz E,Piechal A,Gajkowska B,et al. Tellurium-induced cognitive deficits in rats are related to neuropathological changes in the central nervous system. Toxicol Lett,2002,131:203-14.
[31] Wang K,Gong P,Liu L,et al. Effect of 2-TeCD on the expression of adhesion molecules in human umbilical vein endothelial cells under the stimulation of tumor necrosis factor-alpha. Int Immunopharmacol,2009,9:1087-91.
[32] Ren X,Xue Y,Liu J,et al. A novel cyclodextrin-derived tellurium compound with glutathioneperoxidase activity. Chembiochem,2002,3:356-63.
[33] Cann JR. Theoretical studies on the mobility-shift assay of protein-DNA complexes. Electrophoresis,1998,19:127-41
[2] Kaufmann SH,Steensma DP. On the TRAIL of a new therapy for leukemia. Leukemia,2005,19:2195-202.
[3] Rahman M,Pumphrey JG,Lipkowitz S. The TRAIL to targeted therapy of breast cancer. Adv Cancer Res,2009,103:43-73.
[4] Qiao L,Wong BC. Targeting apoptosis as an approach for gastrointestinal cancer therapy. Drug Resist Updat,2009,12:55-64.
[5] Sheikh MS,Huang Y,Fernandez-Salas EA,et al. The antiapoptotic decoy receptor TRID/TRAIL-R3 is a p53-regulated DNA damage-inducible gene that is overexpressed in primary tumors of the gastrointestinal tract. Oncogene,1999,18:4153-9.
[6] Rosevear HM,Lightfoot AJ,et al. The role of neutrophils and TNF-related apoptosis-inducing ligand(TRAIL)in bacillus Calmette-Guérin(BCG)immunotherapy for urothelial carcinoma of the bladder. Cancer Metastasis Rev,2009,28:345-53.
[7] Hao C,Beguinot F,Condorelli G,et al. Induction and intracellular regulation of tumor necrosis factor-related apoptosis-inducing ligand(TRAIL)mediated apotosis in human malignant glioma cells. Cancer Res,2001,61:1162-70.
[8] Wu M,Das A,Tan Y,et al. Induction of apoptosis in glioma cell lines by TRAIL/Apo-2l. JNeurosci Res,2000,61:464-70.
[9] The potential of death receptor 4- and 5-directed therapies in the treatment of lung cancer. Clin Lung Cancer,2007,8:413-9
[10] Bucur O,Ray S,Bucur MC,Almasan A. APO2 ligand/tumor necrosis factor-related apoptosis- inducing ligand in prostate cancer therapy. Front Biosci,2006,11:1549-68.
[11] Shimada O,Wu X,Jin X,et al. Human agonistic antibody to tumor necrosis factor-related apoptosis-inducing ligand receptor 2 induces cytotoxicity and apoptosis in prostate cancer and bladder cancer cells. Urology,2007,69:395-401.
[12] Bretz JD,Rymaszewski M,Arscott PL,et al. TRAIL death pathway expression and induction in thyroid follicular cells. J Biol Chem,1999,274:23627-32.
[13] Ryu HS,Chang KH,Chang SJ,et al. Expression of TRAIL(TNF-related apoptosis-inducing ligand)receptors in cervical cancer. Int J Gynecol Cancer,2000,10:417-24.
[14] Herr I,Schemmer P,Büchler MW. On the TRAIL to therapeutic intervention in liver disease. Hepatology,2007,46:266-74.
[15] Pfizenmaier K,Wajant H,Grell M. Tumor necrosis factors in 1996. Cytokine Growth Factor,1996,7:271-7.
[16] Walczak H,Krammer PH. The CD95(APO-1/Fas)and the TRAIL(APO-2L)apoptosis systems. Exp Cell Res,2000,256:58-66.
[17] Wiley SR,Schooley K,Smolak PJ,et al. Identification and characterization of a new member of TNF family that induce apoptosis. Immunity,1995,3:673-682.
[18] Seol DW,Billiar TR. Cysteine 230 modulates tumor necrosis factor-relate apoptosis-inducing ligand activity. Cancer Res,2000,60:3152-4.
[19] Hymowitz SG,O'Connell MP,Ultsch MH,et al. A unique zinc-binding site revealed by a high-resolution X-ray structure of homotrimeric Apo2L/TRAIL. Biochemistry,2000 ,39:633-40.
[20] Cha SS,Song YL,Oh BH. Specificity of molecular recognition learned from the crystal structures of TRAIL and the TRAIL: sDR5 complex. Vitam Horm,2004,67:1-17.
[21] Pitti RM,Marsters SA,Ruppert S,et al. Induction of apoptosis by Apo-2 ligand,a new member of the tumor necrosis factor cytokine family. J Biol Chem,1996,271:12687-90.
[22] Griffith TS,Lynch DH. Trail: a molecule with multiple receptor and control mechanisms. Curr Opin Immunol,1998,10:559-563
[23] Pan G,O‘Rourke K,Chinnaiyan AM,et al. The receptor for the cytotoxic ligand TRAIL. Science,1997,276:111–3.
[24] MacFarlane M,Ahmad M,Srinivasula SM,et al. Identification and molecular cloning of twonovel receptors for the cytotoxic ligand TRAIL. J Biol Chem,1997,272:25417-20.
[25] Pan H,Rourke K,chinnaiyan AM,et al. The receptor for the cytotoxic ligand TRAIL. Science,1997,276:1111.
[26] Walczak H,Degli-Esposti MA,Johnson RS,et al. TRAIL-R2: a novel apoptosis-mediating receptor for TRAIL. EMBO J,1997,16:5386-97.
[27] Papenfuss K,Cordier SM,Walczak H. Death receptors as targets for anti-cancer therapy. J Cell Mol Med,2008,12:2566-85.
[28] Elrod HA,Sun SY. Modulation of death receptors by cancer therapeutic agents. Cancer Biol Ther,2008,7:163-73.
[29] Van der Sloot AM,Tur V,Szegezdi E,et al. Designed tumor necrosis factor-related apoptosis-inducing ligand variants initiating apoptosis exclusively via the DR5 receptor. Proc Natl Acad Sci U S A,2006,103:8634-9.
[30] Kelley RF,Totpal K,Lindstrom SH,et al. Receptor-selective mutants of apoptosis-inducing ligand 2/tumor necrosis factor-related apoptosis-inducing ligand reveal a greater contribution of death receptor(DR)5 than DR4 to apoptosis signaling. J Biol Chem,2005,280:2205-12.
[31] Degli-Esposti MA,Smolak PJ,Walczak H,et al. Cloning and characterization of TRAIL-R3,a novel member of the emerging TRAIL receptor family. J Exp Med,1997,186:1165–70.
[32] Merino D,Lalaoui N,Morizot A,et al. Differential inhibition of TRAIL-mediated DR5-DISC formation by decoy receptors 1 and 2. Mol Cell Biol,2006,26:7046–7055.
[33] Marsters SA,Sheridan JP,Pitti RM,et al. A novel receptor for Apo2L/TRAIL contains a truncated death domain. Curr Biol,1997,7:1003–6.
[34] Degli-Esposti MA,Dougall WC,Smolak PJ,et al. The novel receptor TRAIL-R4 induces NF-kB and protects against TRAIL-mediated apoptosis,yet retains an incomplete death domain. Immunity,1997,7:813–20
[35] Clancy L,Mruk K,Archer K,et al. Preligand assembly domain-mediated ligand-independent association between TRAIL receptor 4(TR4)and TR2 regulates TRAIL-induced apoptosis. Proc Natl Acad Sci,2005,102:18099–104.
[36] Zhang XD,Franco AV,Nguyen T,et al. Differential localization and regulation of death and decoy receptors for TNF-relatedapoptosis-inducing ligand(TRAIL)in human melanoma cells. J Immunol,2000,164:3961-70.
[37] Emery JG,McDonnell P,Burke MB,et al. Osteoprotegerin is a receptor for the cytotoxic ligand TRAIL. J Biol Chem,1998,273:14363–7.
[38] Hofbauer LC. Osteoprotegerin ligand and osteoprotegerin: novel implications for osteoclast biology and bone metabolism. Eur J Endocrinol,1999,141:195-210.
[39] Lacey DL,Timms E,Tan HL,et al. Osteoprotegerin ligand is a cytokine that regulates osteoclast differentiation and activation. Cell,1998,93:165–76.
[40] Boatright KM,Renatus M,Scott FL,et al. A unified model for apical Caspase activation. Mol Cell,2003,11:529–41.
[41] Kischkel FC,Lawrence DA,Chuntharapai A. Apo2L/TRAIL-dependent recruitment of endogenous FADD and Caspase-8 to death receptors 4 and5. Immunity,2000,12:611-20.
[42] Kischkel FC,Hellbardt S,Behrmann I,et al. Cytotoxicity-dependent APO-1(Fas/CD95)- associated proteins form a death-inducing signaling complex(DISC)with the receptor. EMBO J,1995,14:5579-88.
[43] Bodmer JL,Holler N,Reynard S. TRAIL receptor-2 signals apoptosis through FADD and Caspase-8. Nat Cell Biol,2000,2:241-3.
[44] Chen Q,Ray S,Hussein MA,et al. Role of Apo2L/TRAIL and Bcl-2-family proteins in apoptosis of multiple myeloma. Leuk Lymphoma,2003,44:1209-14.
[45] Jiang X,Wang X. Cytochrome c promotes Caspase-9 activation by inducing nucleotide binding to Apaf-1. J Biol Chem,2000,275:31199-203.
[46] Du C,Fang M,Li Y,et al. Smac,a mitochondrial protein that promotes cytochrome c-dependent Caspase activation by eliminating IAP inhibition. Cell,2000,102:33-42.
[47] El-Deiry WS. Insights into cancer therapeutic design based on p53 and TRAIL receptor signaling. Cell Death Differ,2001,8:1066-75.
[48] Kim YS,Schwabe RF,Qian T,et al. TRAIL-mediated apoptosis requires NF-kappaB inhibition and the mitochondrial permeability transition in human hepatoma cells. Hepatology,2002,36:1498-508.
[49] Chen X,Kandasamy K,Srivastava RK. Differential roles of RelA(p65)and c-Rel subunits of nuclear factor kappa B in tumor necrosis factor-related apoptosis-inducing ligand signaling. Cancer Res,2003,63:1059-66.
[50] Crook NE,Clem RJ,Miller LK. An apoptosis-inhibiting baculovirus gene with a zinc finger-like motif. J Virol, 1993,67:2168-74.
[51] Deveraux QL,Takahashi R,Salvesen GS,et al. Xlinked IAP is a direct inhibitor of cell - death proteases. Nature 1997,388:300-4.
[52] Duckett CS,Nava VE,Gedrich RW,et al. A conserved family of cellular genes related to the baculovirus iap gene and encoding apoptosis inhibitors. EMBO J,1996,15:2685-94.
[53] Ekert PG,Silke J,Vaux DL. Caspase inhibitors. Cell Death Differ,1999,6:1081-6.
[54] LaCasse EC,Baird S,Korneluk RG,et al. The inhibitors of apoptosis(IAPs)and their emerging role in cancer. Oncogene,1998,17:3247 -59.
[55] Rothe M,Pan MG,Henzel WJ,et al. The TNFR2–TRAF signaling complex contains twonovel proteins related to baculoviral inhibitor of apoptosis proteins. Cell,1995,83:1243–52
[56] Roy N,Deveraux QL,Takahashi R,et al. The c - IAP - 1 and c - IAP - 2 proteins are direct inhibitors of specific Caspases. EMBO J,1997,16:6914– 25.
[57] Verhagen AM,Ekert PG,Pakusch M,et al. Identification of DIABLO,a mammalian protein that promotes apoptosis by binding to and antagonizing IAP proteins. Cell,2000,102:43– 53.
[58] Liston P,Roy N,Tamai K,et al. Suppression of apoptosis in mammalian cells by NAIP and arelated family of IAP genes. Nature,1996,379:349– 53.
[59] Thome M,Schneider P,Hofmann K,et al. Viral FLICE-inhibitory proteins(FLIPs)prevent apoptosis induced by death receptors. Nature,1997,386:517-21.
[60] IrmLer M,Thome M,Hahne M,et al. Inhibition of death receptor signals by cellular FLIP. Nature,1997,388:190-5.
[61] Kim Y,Suh N,Sporn M,et al. An inducible pathway for degradation of FLIP protein sensitizes tumor cells to TRAIL-induced apoptosis. J Biol Chem,2002,277:22320-9.
[62] Thorburn A. Death receptor-induced cell killing. Cell Signal,2004,16:139-44.
[63] Safa AR,Day TW,Wu CH. Cellular FLICE-like inhibitory protein(c-FLIP): a novel target for cancer therapy. Curr Cancer Drug Targets,2008,8:37-46.
[64] Goke R,Goke A,Goke B,et al. Regulation of TRAIL-induced apoptosis by transcription factors. Cell Immunol,2000,201:77-82.
[65] Costanzo A,Guiet C,Vito P. c-E10 is a Caspase-recruiting domain-containing protein that interacts with components of death receptors signaling pathway and activates nuclear factor-kappaB. J Biol Chem,1999,274:20127-32.
[66] Jeremias I,Kupatt C,Baumann B,et al. Inhibition of nuclear factor kappaB activation attenuates apoptosis resistance in lymphoid cells. Blood,1998,91:4624-31.
[67] Lin Y,Devin A,Rodriguez Y,et al. Cleavage of the death domain kinase RIP by Caspase-8 prompts TNF-induced apoptosis. Genes Dev,1999,13:2514-26.
[68] Martinon F,Holler N,Richard C,et al. Activation of a pro-apoptotic amplification loop through inhibition of NF-kappaB-dependent survival signals by Caspase-mediated inactivation of RIP. FEBS Lett,2000,468:134-6.
[69] Harper N , Farrow SN , Kaptein A , et al. Modulation of tumor necrosis factor apoptosis-inducing ligand-induced NF-kappa B activation by inhibition of apical Caspases. J Biol Chem,2001,276:34743-52.
[70] Dai Y,Liu M,Tang W,Li Y,et al. A Smac-mimetic sensitizes prostate cancer cells to TRAIL-induced apoptosis via modulating both IAPs and NF-kappaB. BMC Cancer,2009,9:392.
[71] Festa M,Petrella A,Alfano S,et al. R-roscovitine sensitizes anaplastic thyroid carcinoma cells to TRAIL-induced apoptosis via regulation of IKK/NF-kappaB pathway. Int J Cancer,2009,124:2728-36.
[72] Lee TJ,Jang JH,Noh HJ,et al. Overexpression of Par-4 sensitizes TRAIL-induced apoptosis via inactivation of NF-kappaB and Akt signaling pathways in renal cancer cells. J Cell Biochem,2010,109:885-95.
[73] Benedict CA,Banks TA,Ware CF. Death and survival: viral regulation of TNF signaling pathways. Curr Opin Immunol,2003,15:59-65.
[74] Clarke P,Meintzer SM,Gibson S,et al. Reovirus-induced apoptosis is mediated by TRAIL. J Virol,2000,74:8135-9.
[75] Sedger LM,Shows DM,Blanton RA,et al. IFN-gamma mediates a novel antiviral activity through dynamic modulation of TRAIL and TRAIL receptor expression. J Immunol,1999,163:920-6.
[76] Simmen KA,Singh J,Luukkonen BG,et al. Global modulation of cellular transcription by human cytomegalovirus is initiated by viral glycoprotein B. Proc Natl Acad Sci U S A,2001,98:7140-5.
[77] Shisler J,Yang C,Walter B,et al. The adenovirus E3-10.4K/14.5K complex mediates loss of cell surface Fas(CD95)and resistance to Fas-induced apoptosis. J Virol,1997,71:8299-306.
[78] Benedict CA,Norris PS,Prigozy TI,et al. Three adenovirus E3 proteins cooperate to evade apoptosis by tumor necrosis factor-related apoptosis-inducing ligand receptor-1 and -2. J Biol Chem,2001,276:3270-8.
[79] Thome M,Tschopp J.Regulation of lymphocyte proliferation and death by FLIP. Nat Rev Immunol,2001,1:50-8.
[80] Skaletskaya A,Bartle LM,Chittenden T,et al. A cytomegalovirus-encoded inhibitor of apoptosis that suppresses Caspase-8 activation. Proc Natl Acad Sci U S A,2001,98:7829-34.
[81] Geleziunas R,Xu W,Takeda K,et al. HIV-1 Nef inhibits ASK1-dependent death signalling providing a potential mechanism for protecting the infected host cell. Nature,2001,410:834-8.
[82] Chang HY,Nishitoh H,Yang X,et al. Activation of apoptosis signal-regulating kinase 1(ASK1)by the adapter protein Daxx. Science,1998,281:1860-3.
[83] Adrain C,Martin SJ. The mitochondrial apoptosome: a killer unleashed by the cytochrome seas. Trends Biochem Sci,2001,26:390-7.
[84] Henderson S,Huen D,Rowe M,et al. Epstein-Barr virus-coded BHRF1 protein,a viral homologue of Bcl-2,protects human B cells from programmed cell death. Proc Natl Acad SciU S A,1993,90:8479-83.
[85] Sarid R,Sato T,Bohenzky RA,et al. Kaposi's sarcoma-associated herpesvirus encodes a functional bcl-2 homologue. Nat Med,1997,3:293-8.
[86] Chinnaiyan AM,Prasad U,Shankar S,et al. Combined effect of tumor necrosis factor-related apoptosis-inducing ligand and ionizing radiation in breast cancer therapy. Proc Natl Acad Sci,2000,97:1754-9.
[87] Gong B,Almasan A. Apo2 ligand/TNF-related apoptosis-inducing ligand and death receptor 5 mediate the apoptotic signaling induced by ionizing radiation in leukemic cells. Cancer Res,2000,60:5754-60.
[88] Hori T,Kondo T,Kanamori M,et al. Ionizing radiation enhances tumor necrosis factor-related apoptosis-inducing ligand(TRAIL)-induced apoptosis through up-regulations of death receptor 4(DR4)and death receptor 5(DR5)in human osteosarcoma cells. J Orthop Res,2009.
[89] Keane MM,Ettenberg SA,Nau MM,et al. Chemotherapy augments TRAIL-induced apoptosis in breast cell lines. Cancer Res,1999,59:734-41.
[90] Singh TR,Shankar S,Chen X,et al. Synergistic interactions of chemotherapeutic drugs and tumor necrosis factor-related apoptosis-inducing ligand/Apo-2 ligand on apoptosis and on regression of breast carcinoma in vivo. Cancer Res,2003,63:5390-400.
[91] Ganten TM,Haas TL,Sykora J,et al. Enhanced Caspase-8 recruitment to and activation at the DISC is critical for sensitisation of human hepatocellular carcinoma cells to TRAIL-induced apoptosis by chemotherapeutic drugs. Cell Death Differ,2004,11:S86-96.
[92] Kim KM,Song JJ,An JY,et al. Pretreatment of acetylsalicylic acid promotes tumor necrosis factor-related apoptosis-inducing ligand-induced apoptosis by down-regulating BCL-2 gene expression. J Biol Chem,2005,280:41047-56.
[93] Yoo J,Lee YJ. Aspirin enhances tumor necrosis factor-related apoptosis-inducing ligand-mediated apoptosis in hormone-refractory prostate cancer cells through survivin down-regulation. Mol Pharmacol,2007,72:1586-92.
[94] Lu M,Strohecker A,Chen F,et al. Aspirin sensitizes cancer cells to TRAIL-induced apoptosis by reducing survivin levels. Clin Cancer Res,2008,14:3168-76.
[95] Liu X,Yue P,Zhou Z,et al. Death receptor regulation and celecoxib-induced apoptosis in human lung cancer cells. J Natl Cancer Inst,2004,96:1769-80.
[96] Liu X,Yue P,Sch?nthal AH,et al. Cellular FLICE-inhibitory protein down-regulation contributes to celecoxib-induced apoptosis in human lung cancer cells. Cancer Res,2006,66:11115-9.
[97] He Q,Luo X,Jin W,et al. Celecoxib and a novel COX-2 inhibitor ON09310 upregulate deathreceptor 5 expression via GADD153/CHOP. Oncogene,2008,27:2656-60.
[98] Rushworth SA,Micheau O. Molecular crosstalk between TRAIL and natural antioxidants in the treatment of cancer. Br J Pharmacol,2009,157:1186-8.
[99] Sah NK,Munshi A,Kurland JF,et al. Translation inhibitors sensitize prostate cancer cells to apoptosis induced by tumor necrosis factor-related apoptosis-inducing ligand(TRAIL)by activating c-Jun N-terminal kinase. J Biol Chem,2003,278:20593-602.
[100] Deeb D,Xu YX,Jiang H,et al. Curcumin(diferuloyl-methane)enhances tumor necrosis factor-related apoptosis-inducing ligand-induced apoptosis in LNCaP prostate cancer cells. Mol Cancer Ther,2003,2:95-103.
[101] Deeb D,Jiang H,Gao X,et al. Curcumin sensitizes prostate cancer cells to tumor necrosis factor-related apoptosis-inducing ligand/Apo2L by inhibiting nuclear factor-kappaB through suppression of IkappaBalpha phosphorylation. Mol Cancer Ther,2004,3:803-12.
[102] Deeb DD,Jiang H,Gao X,et al. Chemosensitization of hormone-refractory prostate cancer cells by curcumin to TRAIL-induced apoptosis. J Exp Ther Oncol,2005,5:81-91.
[103] Gao X,Deeb D,Jiang H,et al. Curcumin differentially sensitizes malignant glioma cells to TRAIL/Apo2L-mediated apoptosis through activation of proCaspases and release of cytochrome c from mitochondria. J Exp Ther Oncol,2005,5:39-48
[104] Jung EM,Lim JH,Lee TJ,et al. Curcumin sensitizes tumor necrosis factor-related apoptosis-inducing ligand(TRAIL)-induced apoptosis through reactive oxygen species-mediated upregulation of death receptor 5(DR5). Carcinogenesis,2005,26:1905-13.
[105] Khanbolooki S,Nawrocki ST,Arumugam T,et al. Nuclear factor-kappaB maintains TRAIL resistance in human pancreatic cancer cells. Mol Cancer Ther,2006,5:2251-60.
[106] Jung EM,Park JW,Choi KS,et al. Curcumin sensitizes tumor necrosis factor-related apoptosis-inducing ligand(TRAIL)-mediated apoptosis through CHOP-independent DR5 upregulation. Carcinogenesis,2006,27:2008-17.
[107] Kim H,Kim EH,Eom YW,et al. Sulforaphane sensitizes tumor necrosis factor-related apoptosis-inducing ligand(TRAIL)-resistant hepatoma cells to TRAIL-induced apoptosis through reactive oxygen species-mediated up-regulation of DR5. Cancer Res,2006,66:1740-50.
[108] Kamat AM,Sethi G,Aggarwal BB. Curcumin potentiates the apoptotic effects of chemotherapeutic agents and cytokines through down-regulation of nuclear factor-kappaB and nuclear factor-kappaB-regulated gene products in IFN-alpha-sensitive and IFN-alpha-resistant human bladder cancer cells. Mol Cancer Ther,2007,6:1022-30.
[109] Deeb D,Jiang H,Gao X,et al. Curcumin [1,7-bis(4-hydroxy-3-methoxyphenyl)-1-6-heptadine-3,5-dione; C21H20O6] sensitizes human prostate cancer cells to tumornecrosis factor-related apoptosis-inducing ligand/Apo2L-induced apoptosis by suppressing nuclear factor-kappaB via inhibition of the prosurvival Akt signaling pathway. J Pharmacol Exp Ther,2007,321:616-25.
[110] Wahl H,Tan L,Griffith K,et al. Curcumin enhances Apo2L/TRAIL-induced apoptosis in chemoresistant ovarian cancer cells. Gynecol Oncol,2007,105:104-12.
[111] Srivastava RK,Chen Q,Siddiqui I,et al. Linkage of curcumin-induced cell cycle arrest and apoptosis by cyclin-dependent kinase inhibitor p21(/WAF1/CIP1). Cell Cycle,2007,6:2953-61
[112] Andrzejewski T,Deeb D,Gao X,et al. Therapeutic efficacy of curcumin/TRAIL combination regimen for hormone-refractory prostate cancer. Oncol Res,2008,17:257-67.
[113] Teiten MH,Gaascht F,Eifes S,et al. Chemopreventive potential of curcumin in prostate cancer.Genes Nutr,2009 Oct 6.
[114] Shankar S,Ganapathy S,Chen Q,et al. Curcumin sensitizes TRAIL-resistant xenografts: molecular mechanisms of apoptosis,metastasis and angiogenesis. Mol Cancer,2008,7:16.
[115] Kamat AM,Tharakan ST,Sung B,et al. Curcumin potentiates the antitumor effects of Bacillus Calmette-Guerin against bladder cancer through the downregulation of NF-kappaB and upregulation of TRAIL receptors. Cancer Res,2009,69:8958-66.
[116] Kim H,Kim EH,Eom YW,et al. Sulforaphane sensitizes tumor necrosis factor-related apoptosis-inducing ligand(TRAIL)-resistant hepatoma cells to TRAIL-induced apoptosis through reactive oxygen species-mediated up-regulation of DR5. Cancer Res,2006,66:1740-50.
[117] Shankar S,Ganapathy S,Srivastava RK. Sulforaphane enhances the therapeutic potential of TRAIL in prostate cancer orthotopic model through regulation of apoptosis,metastasis,and angiogenesis. Clin Cancer Res,2008,14:6855-66.
[118] Jin CY,Moon DO,Lee JD,et al. Sulforaphane sensitizes tumor necrosis factor-related apoptosis-inducing ligand-mediated apoptosis through downregulation of ERK and Akt in lung adenocarcinoma A549 cells. Carcinogenesis,2007,28:1058-66.
[119] Shankar S,Ganapathy S,Srivastava RK. Sulforaphane enhances the therapeutic potential of TRAIL in prostate cancer orthotopic model through regulation of apoptosis,metastasis,and angiogenesis. Clin Cancer Res,2008,14:6855-66.
[120] Kallifatidis G,Rausch V,Baumann B,et al. Sulforaphane targets pancreatic tumour-initiating cells by NF-kappaB-induced antiapoptotic signalling. Gut,2009,58:949-63.
[121] Jin CY,Moon DO,Lee JD,et al. Sulforaphane sensitizes tumor necrosis factor-related apoptosis-inducing ligand-mediated apoptosis through downregulation of ERK and Akt in lung adenocarcinoma A549 cells. Carcinogenesis,2007,28:1058-66.
[122] Matsui TA,Sowa Y,Yoshida T,et al. Sulforaphane enhances TRAIL-induced apoptosis through the induction of DR5 expression in human osteosarcoma cells. Carcinogenesis,2006,27:1768-77.
[123] Toppo S,FlohéL,Ursini F,et al. Catalytic mechanisms and specificities of glutathione peroxidases: variations of a basic scheme. Biochim Biophys Acta,2009,1790:1486-500.
[124] Brigelius-FlohéR,Kipp A. Glutathione peroxidases in different stages of carcinogenesis. Biochim Biophys Acta,2009,1790:1555-68.
[125] Steinbrenner H,Sies H. Protection against reactive oxygen species by selenoproteins. Biochim Biophys Acta,2009,1790:1478-85.
[126] Brigelius-FlohéR. Glutathione peroxidases and redox-regulated transcription factors. Biol Chem, 2006,387:1329-35.
[127] Bartel J,Bartz T,Wolf C,et al. Activity of the glutathione peroxidase-2. Differences in the selenium-dependent expression between colon and small intestine. Cancer Genomics Proteomics,2007,4:369-72.
[128] Ottaviano FG,Tang SS,Handy DE,et al. Regulation of the extracellular antioxidant selenoprotein plasma glutathione peroxidase(GPx-3)in mammalian cells. Mol Cell Biochem,2009,327:111-26.
[129] Ding WQ,Lind SE,Phospholipid hydroperoxide glutathione peroxidase plays a role in protecting cancer cells from docosahexaenoic acid-induced cytotoxicity. Mol Cancer Ther,2007,6:1467-74.
[130] Meseguer M,Martínez-Conejero JA,et al. The human sperm glutathione system: a key role in male fertility and successful cryopreservation. Drug Metab Lett,2007,1:121-6.
[131] Namura S,Nagata I,Takami S,et al. Ebselen reduces cytochrome c release from mitochondria and subsequent DNA fragmentation after transient focal cerebral ischemia in mice. Stroke,2001,32:1906-11.
[132] Kotamraju S,Konorev EA,Joseph J,et al. Doxorubicin-induced apoptosis in endothelial cells and cardiomyocytes is ameliorated by nitrone spin traps and ebselen. Role of reactive oxygen and nitrogen species. J Biol Chem,2000,275:33585-92.
[133] Tanaka M,Takezawa N,Kumai T,et al. Ebselen protects against the reduction in levels of drug-metabolizing enzymes in livers of rats with deoxycholic acid-induced liver injury. Pharmacol Toxicol,2002,91:64-70.
[134] Wasser S,Lim GY,Ong CN,et al. Anti-oxidant ebselen causes the resolution of experimentally induced hepatic fibrosis in rats. J Gastroenterol Hepatol,2001,16:1244-53.
[135] Wu Q,Huang K. Effect of selenium compounds on the damage induced by oxysterol on ratarterial walls. Biol Trace Elem Res,2006,112:273-82.
[136] Engman L,Cotgreave I,Angulo M,et al. Diaryl chalcogenides as selective inhibitors of thioredoxin reductase and potential antitumor agents. Anticancer Res,1997,17:4599-605.
[137] Yang CF,Shen HM,Ong CN. Ebselen induces apoptosis in HepG(2)cells through rapid depletion of intracellular thiols. Arch Biochem Biophys,2000,374:142-52.
[138] Sharma V,Tewari R,Sk UH,et al. Ebselen sensitizes glioblastoma cells to Tumor Necrosis Factor(TNFalpha)-induced apoptosis through two distinct pathways involving NF-kappaB downregulation and Fas-mediated formation of death inducing signaling complex. Int J Cancer,2008,123:2204-12
[139] Sun Y,Mu Y,Ma S ,et al. The molecular mechanism of protecting cells against oxidative stress by 2-selenium-bridged beta-cyclodextrin with glutathione peroxidase activity. Biochim Biophys Acta,2005,1743:199-204.
[140] Jia ZD,Mu Y,Yan GL,et al. Comparison between the effects of 2-selenium-bridged beta-cyclodextrin and ebselen on treating SHRsp stroke. Chem Res Chinese U,2008,24:1–8.
[141] Lin TT,Wang BM,Li XY,et al. An insight into the protection of rat liver against ischemia/reperfusion injury by 2-selenium-bridged beta-cyclodextrin. Hepatol Res,2009,39:1125-36
[142] Wang BM(王冰梅). Studies on the Anti-tumor Effects of the two GPX Mimics and their action Mechanisms,PhD Thesis,Jilin University,2007.
[143] Wang K,Gong P,Liu L,et al. Effect of 2-TeCD on the expression of adhesion molecules in human umbilical vein endothelial cells under the stimulation of tumor necrosis factor-alpha. Int Immunopharmacol,2009,9:1087-91.
[144] McNaughton M,Engman L,Birmingham A,et al. Cyclodextrin-derived diorganyl tellurides as glutathione peroxidase mimics and inhibitors of thioredoxin reductase and cancer cell growth. J Med Chem,2004,47:233-9.
[1] Sies H. Ebselen,a selenoorganic compound as glutathione peroxidase mimic. Free Radic Biol Med,1993,14:313-23.
[2] Moussaoui S,Obinu MC,Daniel N,et al. The antioxidant ebselen prevents neurotoxicity and clinical symptoms in a primate model of Parkinson's disease. Exp Neurol,2000,166:235-45.
[3] Konz KH,Tiegs G,Wendel A. Protection by ebselen against endotoxin shock in rats or mice sensitized by galactosamine. Prog Clin Biol Res,1987,236A:281-8.
[4] Namura S,Nagata I,Takami S,et al. Ebselen reduces cytochrome c release from mitochondria and subsequent DNA fragmentation after transient focal cerebral ischemia in mice. Stroke, 2001,32:1906-11.
[5] Cotgreave IA,Johansson U,Westergren G,et al. The anti-inflammatory activity of ebselen but not thiols in experimental alveolitis and bronchiolitis. Agents Actions,1988,24:313-9.
[6] Gao JX,Issekutz AC. The effect of ebselen on polymorphonuclear leukocyte and lymphocyte migration to inflammatory reactions in rats. Immunopharmacology,1993,25:239-51.
[7] MJ Parnham,S Leyck,P Kuhl,J,et al. Ebselen:a new approach to the inhibition of peroxide-dependent inflammation. Int J Tissue React,1987,9:45-50.
[8] Yamaguchi T. Phase III trial of Ebselen. The American Stroke Association 28th International Stroke Conference,Phoenix,Arizona,2003. p. CTP20.
[9] Yang CF,Shen HM,Ong CN. Ebselen induces apoptosis in HepG(2)cells through rapid depletion of intracellular thiols. Arch Biochem Biophys,2000,374:142-52.
[10] Sharma V,Tewari R,Sk UH,et al. Ebselen sensitizes glioblastoma cells to Tumor NecrosisFactor(TNFalpha)-induced apoptosis through two distinct pathways involving NF-kappaB downregulation and Fas-mediated formation of death inducing signaling complex. Int J Cancer,2008,123:2204-12
[11] Suzuki K.Anti-oxidants for therapeutic use: why are only a few drugs in clinical use?Adv Drug Deliv Rev,2009,61:287-9.
[12] Sun Y,Mu Y,Ma S,et al. The molecular mechanism of protecting cells against oxidative stress by 2-selenium-bridged beta-cyclodextrin with glutathione peroxidase activity. Biochim Biophys Acta,2005,1743:199-204.
[13] Lin TT,Wang BM,Li XY,et al. An insight into the protection of rat liver against ischemia/reperfusion injury by 2-selenium-bridged beta-cyclodextrin. Hepatol Res,2009,39:1125-36
[14] Jia ZD,Mu Y,Yan GL, et al. Comparison between the effects of 2-selenium-bridged beta-cyclodextrin and ebselen on treating SHRsp stroke. Chem Res Chinese U,2008,24:1–8.
[15] Wang BM.(王冰梅)Studies on the Anti-tumor Effects of the two GPX Mimics and their action Mechanisms,PhD Thesis,Jilin University,2007.
[16] Wang K,Gong P,Liu L,et al. Effect of 2-TeCD on the expression of adhesion molecules in human umbilical vein endothelial cells under the stimulation of tumor necrosis factor-alpha. Int Immunopharmacol,2009,9:1087-91.
[17] McNaughton M,Engman L,Birmingham A,et al. Cyclodextrin-derived diorganyl tellurides as glutathione peroxidase mimics and inhibitors of thioredoxin reductase and cancer cell growth. J Med Chem,2004,47:233-9.
[18] Keane MM,Ettenberg SA,Nau MM,et al. Chemotherapy augments TRAIL-induced apoptosis in breast cell lines. Cancer Res,1999,59:734-41.
[19] Singh TR,Shankar S,Chen X,et al. Synergistic interactions of chemotherapeutic drugs and tumor necrosis factor-related apoptosis-inducing ligand/Apo-2 ligand on apoptosis and on regression of breast carcinoma in vivo. Cancer Res,2003,63:5390-400.
[20] Yamaguchi K,Uzzo RG,Pimkina J,et al. Methylseleninic acid sensitizes prostate cancer cells to TRAIL-mediated apoptosis. Oncogene,2005,24:5868-77.
[21] Hu H,Jiang C,Schuster T,Li GX,et al. Inorganic selenium sensitizes prostate cancer cells to TRAIL-induced apoptosis through superoxide/p53/Bax-mediated activation of mitochondrial pathway. Mol Cancer Ther,2006,5:1873-82.
[22] Kretz-Remy C,Mehlen P,Mirault ME,et al. Inhibition of IkB-a phosphorylation and degradation and subsequent NF-kB activation by glutathione peroxidase overexpression. J Cell Biol,1996,133:1083–93.
[23] Rygaard J,Povlsen CO. Heterotransplantation of a human malignant tumour to "Nude" mice. Acta Pathol Microbiol Scand,1969,77:758-60.
[24] Rygaard J. Immunobiology of the mouse mutant "Nude". Preliminary investigations. Acta Pathol Microbiol Scand,1969,77:761-2.
[25] Meotti FC,Borges VC,Zeni G,et al. Potential renal and hepatic toxicity of diphenyl diselenide,diphenyl ditelluride and Ebselen for rats and mice. Toxicol Lett,2003,143:9-16.
[26] Widy-Tyszkiewicz E,Piechal A,Gajkowska B,et al. Tellurium-induced cognitive deficits in rats are related to neuropathological changes in the central nervous system. Toxicol Lett,2002,131:203-14.
[1] Degli-Esposti M. To die or not to die--the quest of the TRAIL receptors. J Leukoc Biol,1999,65:535-42.
[2] Kischkel FC,Hellbardt S,Behrmann I,et al. Cytotoxicity-dependent APO-1(Fas/CD95)- associated proteins form a death-inducing signaling complex(DISC)with the receptor. EMBO J,1995,14:5579-88.
[3] Kischkel FC,Lawrence DA,Chuntharapai A,et al. Apo2L/TRAIL-dependent recruitment of endogenous FADD and Caspase-8 to death receptors 4 and 5. Immunity,2000,12:611-20.
[4] Kim YS,Schwabe RF,Qian T,et al. TRAIL-mediated apoptosis requires NF-kappaB inhibition and the mitochondrial permeability transition in human hepatoma cells. Hepatology,2002,36:1498-508.
[5] Kreuz S,Siegmund D,Scheurich P,et al. NF-kappaB inducers upregulate cFLIP,a cycloheximide-sensitive inhibitor of death receptor signaling. Mol Cell Biol , 2001 ,21:3964-73.
[6] Rahman M,Pumphrey JG,Lipkowitz S. The TRAIL to targeted therapy of breast cancer. Adv Cancer Res,2009,103:43-73.
[7] Keane MM,Ettenberg SA,Nau MM,et al. Chemotherapy augments TRAIL-induced apoptosis in breast cell lines. Cancer Res,1999,59:734-41.
[8] Singh TR,Shankar S,Chen X,et al. Synergistic interactions of chemotherapeutic drugs and TRAIL /Apo-2 ligand on apoptosis and on regression of breast carcinoma in vivo. Cancer Res,2003,63:5390-400.
[9] Ganten TM,Koschny R,Sykora J,et al. Preclinical differentiation between apparently safe and potentially hepatotoxic applications of TRAIL either alone or in combination with chemotherapeutic drugs. Clin Cancer Res,2006,12:2640-6.
[10] Koschny R,Ganten TM,Sykora J,et al. TRAIL/bortezomib cotreatment is potentiallyhepatotoxic but induces cancer-specific apoptosis within a therapeutic window. Hepatology,2007,45:649-58.
[11] Jia ZD,Mu Y,Yan GL,et al. Comparison between the effects of 2-selenium-bridged beta-cyclodextrin and ebselen on treating SHRsp stroke. Chem Res Chinese U,2008,24:1–8.
[12] Liu J,Luo G,Ren X,et al. A bis-cyclodextrin diselenide with glutathione peroxidase-like activity. Biochim Biophys Acta,2000,1481:222-8.
[13] Sun Y,MuY,Ma S,et al. The molecular mechanism of protecting cells against oxidative stress by 2-selenium-bridged beta-cyclodextrin with glutathione peroxidase activity. Biochim Biophys Acta,2005,1743:199-204.
[14] Yamaguchi K,Uzzo RG,Pimkina J,et al. Methylseleninic acid sensitizes prostate cancer cells to TRAIL-mediated apoptosis. Oncogene,2005,24:5868-77.
[15] Hu H,Jiang C,Schuster T,Li GX,Daniel PT,LüJ. Inorganic selenium sensitizes prostate cancer cells to TRAIL-induced apoptosis through superoxide/p53/Bax-mediated activation of mitochondrial pathway. Mol Cancer Ther,2006,5:1873-82.
[16] Venkateswaran V,Klotz LH,Fleshner NE. Selenium modulation of cell proliferation and cell cycle biomarkers in human prostate carcinoma cell lines. Cancer Res,2002,62:2540-5.
[17] Madhunapantula SV,Desai D,Sharma A,Huh SJ,Amin S,Robertson GP. PBISe,a novel selenium-containing drug for the treatment of malignant melanoma. Mol Cancer Ther,2008,7:1297-308.
[18] Hyer ML,Croxton R,Krajewska M,et al. Synthetic triterpenoids cooperate with TRAIL to induce apoptosis of breast cancer cells. Cancer Res,2005,65:4799-808.
[19] Walczak H,Haas TL. Biochemical analysis of the native TRAIL death-inducing signaling complex. Methods Mol Biol,2008,414:221-39.
[20] Keane MM,Rubinstein Y,Cuello M,et al. Inhibition of NF-kappaB activity enhances TRAIL mediated apoptosis in breast cancer cell lines. Breast Cancer Res Treat,2000,64:211-9.
[21] Yamanaka T,Shiraki K,Sugimoto K,et al. Chemotherapeutic agents augment TRAIL-induced apoptosis in human hepatocellular carcinoma cell lines. Hepatology,2000,32:482-90.
[22] Yu R,Mandlekar S,Ruben S,Ni J,et al. TRAIL-mediated apoptosis in androgen-independent prostate cancer cells. Cancer Res,2000,60:2384-9.
[23] Yeh CC,Deng YT,Sha DY,et al. Suberoylanilide hydroxamic acid sensitizes human oral cancer cells to TRAIL-induced apoptosis through increase DR5 expression. Mol Cancer Ther,2009,8:2718-25.
[24] Zou W,Yue P,Khuri FR,et al. Coupling of endoplasmic reticulum stress to CDDO-Me induced up-regulation of death receptor 5 via a CHOP-dependent mechanism involving JNKactivation. Cancer Res,2008,68:7484-92.
[25] Lu M,Xia L,Hua H,et al. Acetyl-keto-beta-boswellic acid induces apoptosis through a death receptor 5-mediated pathway in prostate cancer cells. Cancer Res,2008,68:1180-6.
[26] Son YG,Kim EH,Kim JY,et al. Silibinin sensitizes human glioma cells to TRAIL-mediated apoptosis via DR5 up-regulation and down-regulation of c-FLIP and survivin. Cancer Res,2007,67:8274-84.
[27] Ghosh S,Baltimore D. Activation in vitro of NF-kappa B by phosphorylation of its inhibitor I kappa B. Nature,1990,344:678-82.
[28] Beg AA,Ruben SM,Scheinman RI,et al. I kappa B interacts with the nuclear localization sequences of the subunits of NF-kappa B: a mechanism for cytoplasmic retention. Genes Dev,1992,6:1899-913.
[29] Oya M,Ohtsubo M,Takayanagi A,et al. Constitutive activation of nuclear factor-kappaB prevents TRAIL-induced apoptosis in renal cancer cells. Oncogene,2001,20:3888-96.
[30] Khanbolooki S,Nawrocki ST,Arumugam T,et al. Nuclear factor-kappaB maintains TRAIL resistance in human pancreatic cancer cells. Mol Cancer Ther,2006,5:2251-60.
[31] Li S,Yan T,Yang JQ,Oberley TD,et al. The role of cellular glutathione peroxidase redox regulation in the suppression of tumor cell growth by manganese superoxide dismutase. Cancer Res,2000,60:3927-39.
[32] Brar SS,Kennedy TP,Whorton AR,et al. Reactive oxygen species from NAD(P)H:quinone oxidoreductase constitutively activate NF-kappaB in malignant melanoma cells. Am J Physiol Cell Physiol,2001,280:C659-76.
[33] Kretz-Remy C,Mehlen P,Mirault ME,et al. Inhibition of IkB-a phosphorylation and degradation and subsequent NF-kB activation by glutathione peroxidase overexpression. J Cell Biol,1996,133:1083–93.
[34] Li Q,Sanlioglu S,Li S,et al. GPx-1 gene delivery modulates NFkappaB activation following diverse environmental injuries through a specific subunit of the IKK complex. Antioxid Redox Signal,2001,3:415-32.
[1] Rygaard J. Immunobiology of the mouse mutant "Nude". Preliminary investigations. Acta Pathol Microbiol Scand,1969,77:761-2.
[2] Giovanella BC. Experimental chemotherapy of human tumors heterotransplanted in nude mice. Antibiot Chemother,1980,28:21-7.
[3] Giovanella BC,Fogh J. The nude mouse in cancer research. Adv Cancer Res,1985,44:69-120.
[4] Dorsey JF,Mintz A,Tian X,et al. Tumor necrosis factor-related apoptosis-inducing ligand(TRAIL)and paclitaxel have cooperative in vivo effects against glioblastoma multiforme cells. Mol Cancer Ther, 2009,8:3285-95.
[5] Shankar S,Davis R,Singh KP,et al. Suberoylanilide hydroxamic acid(Zolinza/vorinostat)sensitizes TRAIL-resistant breast cancer cells orthotopically implanted in BALB/c nude mice.Mol Cancer Ther,2009,8:1596-605.
[6] Zhang X,Li W,Olumi AF. Low-dose 12-O-tetradecanoylphorbol-13-acetate enhances tumor necrosis factor related apoptosis-inducing ligand induced apoptosis in prostate cancer cells. Clin Cancer Res,2007,13:7181-90.
[7] Hyer ML,Croxton R,Krajewska M,et al. Synthetic triterpenoids cooperate with tumor necrosis factor-related apoptosis-inducing ligand to induce apoptosis of breast cancer cells. Cancer Res,2005,65:4799-808.
[8] Shankar S,Chen X,Srivastava RK. Effects of sequential treatments with chemotherapeutic drugs followed by TRAIL on prostate cancer in vitro and in vivo. Prostate,2005,62:165-86.
[9] Singh TR,Shankar S,Chen X,et al. Synergistic interactions of chemotherapeutic drugs and tumor necrosis factor-related apoptosis-inducing ligand/Apo-2 ligand on apoptosis and on regression of breast carcinoma in vivo. Cancer Res,2003,63:5390-400.
[10] Moldovan GL,Pfander B,Jentsch S. PCNA,the maestro of the replication fork. Cell,2007,129:665-79.
[11] Esteva FJ,Hortobagyi GN. Prognostic molecular markers in early breast cancer. Breast Cancer Res. Breast Cancer Res, 2004,6:109-18.
[12] Scholzen T,Gerdes J. The Ki-67 protein: from the known and the unknown. J Cell Physiol,2000,182:311-22.
[13] Allen RT,Hunter WJ 3rd,Agrawal DK. Morphological and biochemical characterization and analysis of apoptosis. J Pharmacol Toxicol Methods,1997,37:215-28.
[14] Walker RA. Immunohistochemical evaluation of tumours. Curr Opin Immunol,1989,1:878-82.
[1] W?hler F,Justus Liebigs. Ann. Chem. 1840,35: 111.
[2] Andersson CM,Brattsand R,Hallberg A,et al. Diaryl tellurides as inhibitors of lipid peroxidation in biological and chemical systems. Free Radic Res,1994,20:401-10.
[3] Engman L,Stern D,Frisell H ,et al. Synthesis,antioxidant properties,biological activity and molecular modelling of a series of chalcogen analogues of the 5-lipoxygenase inhibitor DuP 654. Bioorg Med Chem,1995,3:1255-62.
[4] Wieslander E,Engman L,Svensj? E,et al. Antioxidative properties of organotellurium compounds in cell systems. Biochem Pharmacol,1998,55:573-84.
[5] Tiano L,Fedeli D,Santroni AM,et al. Effect of three diaryl tellurides,and an organoselenium compound in trout erythrocytes exposed to oxidative stress in vitro. Mutat Res,2000,464:269-77.
[6] Engman L,Gupta V. Tetrahydrofuran Derivatives from Epoxides via Group Transfer Cyclization or Reductive Radical Cyclization of Organotellurium and Organoselenium Intermediates. J Org Chem,1997,62:157-173.
[7] Malmstr?m J , Jonsson M , Cotgreave IA , et al. The antioxidant profile of 2 ,3-dihydrobenzo[b]furan-5-ol and its 1-thio,1-seleno,and 1-telluro analogues. J Am Chem Soc, 2001,123:3434-40.
[8] Sredni B,Caspi RR,Lustig S,et al. The biological activity and immunotherapeutic properties of AS-101,a synthetic organotellurium compound. Nat Immun Cell Growth Regul,1988,7:163-8.
[9] Sredni B,Caspi RR,Klein A,et al. A new immunomodulating compound(AS-101)with potential therapeutic application. Nature,1987,330:173-6.
[10] Shani A,Tichler T,Catane R,et al. Immunologic effects of AS101 in the treatment of cancer patients. Nat Immun Cell Growth Regul,1990,9:182-90.
[11] Kalechman Y,Sotnik-Barkai I,Albeck M,et al. Protection of bone marrow stromal cells from the toxic effects of cyclophosphamide in vivo and of ASTA-Z 7557 and etoposide in vitro by ammonium trichloro(dioxyethylene-O-O')tellurate(AS101). Cancer Res,1993,53:1838-44.
[12] Kalechman Y,Gafter U,Barkai IS,et al. Mechanism of radioprotection conferred by the immunomodulator AS101. Exp Hematol,1993,21:150-5.
[13] Kalechman Y,Sotnik-Barkai I,Albeck M,et al. The effect of AS101 on the reconstitution of T-cell reactivity following irradiation or cyclophosphamide treatment. Exp Hematol,1992,20:1302-8.
[14] Kalechman Y,Albeck M,Sredni B. In vivo synergistic effect of the immunomodulator AS101 and the PKC inducer bryostatin. Cell Immunol,1992,143:143-53.
[15] Kalechman Y,Barkai IS,Albeck M,et al. Use and mechanism of action of AS101 in protecting bone marrow colony forming units-granulocyte-macrophage following purging with ASTA-Z 7557. Cancer Res,1991,51:5614-20.
[16] Kalechman Y,Albeck M,Oron M,et al. Protective and restorative role of AS101 in combination with chemotherapy. Cancer Res,1991,51:1499-503.
[17] Kalechman Y,Albeck M,Oron M,et al. Radioprotective effects of the immunomodulator AS101, J Immunol,1990,145:1512-7.
[18] Sredni B,Kalechman Y,Albeck M,et al. Cytokine secretion effected by synergism of theimmunomodulator AS101 and the protein kinase C inducer bryostatin. Immunology,1990,70:473-7.
[19] Kalechman Y,Shani A,Albeck M,et al. Induction of acute phase proteins in mice and humans by treatment with AS101 , an immunomodulator with radioprotective properties. Immunopharmacology,1995,29:149-58.
[20] Sailer BL,Liles N,Dickerson S,et al. Organotellurium compound toxicity in a promyelocytic cell line compared to non-tellurium-containing organic analog. Toxicol In Vitro,2004,18:475-82.
[21] Sailer BL,Liles N,Dickerson S,et al. Cytometric determination of novel organotellurium compound toxicity in a promyelocytic(HL-60)cell line. Arch Toxicol,2003,77:30-6.
[22] Urig S,Becker K. On the potential of thioredoxin reductase inhibitors for cancer therapy. Semin Cancer Biol,2006,16:452-65.
[23] Pennington JD,Jacobs KM,Sun L,et al. Thioredoxin and thioredoxin reductase as redox-sensitive molecular targets for cancer therapy. Curr Pharm Des,2007,13:3368-77.
[24] Engman L,Kandra T,Gallegos A,et al. Water-soluble organotellurium compounds inhibit thioredoxin reductase and the growth of human cancer cells. Anticancer Drug Des,2000,15:323-30.
[25] Engman L,Al-Maharik N,McNaughton M,et al. Thioredoxin reductase and cancer cell growth inhibition by organotellurium antioxidants. Anticancer Drugs,2003,14:153-61.
[26] Laden BP,Porter TD,et al. Inhibition of human squalene monooxygenase by tellurium compounds: evidence of interaction with vicinal sulfhydryls. J Lipid Res,2001,42:235-40
[27] Goodrum JF. Role of organotellurium species in tellurium neuropathy. Neurochem Res,1998,23:1313-9.
[28] Borges VC,Rocha JB,Nogueira CW. Effect of diphenyl diselenide,diphenyl ditelluride and ebselen on cerebral Na(+),K(+)-ATPase activity in rats. Toxicology,2005,215:191-7.
[29] Meotti FC,Borges VC,Zeni G,et al. Potential renal and hepatic toxicity of diphenyl diselenide,diphenyl ditelluride and Ebselen for rats and mice. Toxicol Lett,2003,143:9-16.
[30] Widy-Tyszkiewicz E,Piechal A,Gajkowska B,et al. Tellurium-induced cognitive deficits in rats are related to neuropathological changes in the central nervous system. Toxicol Lett,2002,131:203-14.
[31] Wang K,Gong P,Liu L,et al. Effect of 2-TeCD on the expression of adhesion molecules in human umbilical vein endothelial cells under the stimulation of tumor necrosis factor-alpha. Int Immunopharmacol,2009,9:1087-91.
[32] Ren X,Xue Y,Liu J,et al. A novel cyclodextrin-derived tellurium compound with glutathioneperoxidase activity. Chembiochem,2002,3:356-63.
[33] Cann JR. Theoretical studies on the mobility-shift assay of protein-DNA complexes. Electrophoresis,1998,19:127-41