GSK-3β和E-cadherin在子宫内膜腺癌中的表达和意义
|
摘要
目的研究糖原合成酶激酶-3(GSK-3β)和E-钙粘蛋白(E-cadherin)在子宫内膜腺癌组织中的表达水平,了解其表达水平与生物学特性、预后的关联。方法应用免疫组织化学SP技术检测55例子宫内膜腺癌组织,19例子宫内膜不典型增生组织,12例正常增殖期子宫内膜组织中GSK-3β和E-cadherin的表达。结果在子宫内膜腺癌组织、子宫内膜不典型增生组织和正常增殖期子宫内膜组织中GSK-3β和E-cadherin的阳性表达呈逐渐增高趋势,差异有统计学意义(χ2=15.640,P=0.000)。GSK-3β在子宫内膜腺癌组织中的表达随患者FIGO分期的进展呈下降趋势(P<0.05),而与组织学病理分级、是否浸润肌层、淋巴结转移、年龄无明显相关(P>0.05);E-cadherin在子宫内膜腺癌组织中的表达随患者组织学病理分级的增高呈下降趋势(P<0.05),而与临床分期、淋巴结转移、是否浸润肌层、年龄无明显相关(P>0.05)。GSK-3β和E-cadherin的表达呈正相关(r=0.516,P=0.000)。结论 GSK-3β和E-cadherin可能在子宫内膜腺癌发生、发展中发挥着既独立又协同的抑癌基因作用。
Objective To investigate the expression of GSK-3β and E-cadherin in human endometrial adenocarcinoma(EAC)and analyze their relationship with clinicopathological features.Methods The GSK-3β and E-cadherin protein in normal proliferative endometrium group(12 cases),endometrial atypical hyperplasia group(19 cases),endometrial adenocarcinoma group(55 cases)were detected by immunohistochemical SP technique.Results The positive expression rates of GSK-3β protein and E-cadherin protein increased gradually in normal proliferative endometrium,endometrial atypical hyperplasia,endometrial adenocarcinoma tissues,and there were statistically significant differences among three groups(χ2=15.640,P=0.000).The positive expression of GSK-3β decreased with the increasing clinical stages(P<0.05),and no difference among pathological grading,age,lymph node metastasis and cancerous tissue infiltration depth(P>0.05).The positive expression of E-cadherin decreased with the increasing histological grade(P<0.05),and no difference between the expression of E-cadherin and clinical stages,myometrial invasion,lymph node metastasis and age(P>0.05).GSK-3β and E-cadherin expression in endometrial carcinoma showed a positive correlation(r=0.516,P=0.000).Conclusion GSK-3β and E-cadherin may play an independent and congenerous anti-oncogene role in the incidence and development of endometrial carcinogenesis.
Objective To investigate the expression of GSK-3β and E-cadherin in human endometrial adenocarcinoma(EAC)and analyze their relationship with clinicopathological features.Methods The GSK-3β and E-cadherin protein in normal proliferative endometrium group(12 cases),endometrial atypical hyperplasia group(19 cases),endometrial adenocarcinoma group(55 cases)were detected by immunohistochemical SP technique.Results The positive expression rates of GSK-3β protein and E-cadherin protein increased gradually in normal proliferative endometrium,endometrial atypical hyperplasia,endometrial adenocarcinoma tissues,and there were statistically significant differences among three groups(χ2=15.640,P=0.000).The positive expression of GSK-3β decreased with the increasing clinical stages(P<0.05),and no difference among pathological grading,age,lymph node metastasis and cancerous tissue infiltration depth(P>0.05).The positive expression of E-cadherin decreased with the increasing histological grade(P<0.05),and no difference between the expression of E-cadherin and clinical stages,myometrial invasion,lymph node metastasis and age(P>0.05).GSK-3β and E-cadherin expression in endometrial carcinoma showed a positive correlation(r=0.516,P=0.000).Conclusion GSK-3β and E-cadherin may play an independent and congenerous anti-oncogene role in the incidence and development of endometrial carcinogenesis.
引文
[1]BURKE W M,ORR J.Endometrial cancer:a review and current management strategies:partⅠ[J].Gynecol Oncol,2014,134(2):385-392.
[2]SIEGEL R,MA J,ZOU Z,et al.Cancer statistics,2014[J].CA cancer J Clin,2014,64(1):9-29.
[3]SIEGEL R L,MILLER K D,JEMAL A.Cancer statistics,2015[J].CA Cancer J Clin,2015,65(1):5-29.
[4]SIEGEL R L,MILLER K D,JEMAL A.Cancer statistics,2016[J].CA Cancer J Clin,2016,66(1):7-30.
[5]DUZYJ C M,BUHIMSCHI I A,MOTAWEA H,et al.The invasive phenotype of placenta accreta extravillous trophoblasts associates with loss of E-cadherin[J].Placenta,2015,36(6):645-651.
[6]YAN D,AVTANSKI D,SAXENA N K,et al.Leptin-induced epithelial-mesenchymal transition in breast cancer cells requiresβ-catenin activation via Akt/GSK3-and MTal/Wnt1 protein-dependent pathways[J].J BiolChem,2012,287(11):8598-8612.
[7]SOKOLOSKY M,CHAPPELL W H,STADELMAN K,et al.Inhibition of GSK-3beta activity can result in drug and hormonal resistance and alter sensitivity to targeted therapy in MCF-7breast cancer cells[J].Cell Cycle,2014,13(5):820-833.
[8]马竹君,冯红超,宋宇峰,等.GSK-3β、E-cadherin、Cytokeratin在口腔鳞状细胞癌中的表达及意义[J].贵州医药,2016,40(4):354-357.
[9]侯新新,赵萌,张贵宇.PPAR7基因表达对子宫内膜癌细胞迁移、侵袭及增殖能力的影响[J].中华妇产科杂志,2014,49(5):360-365.
[10]胡福清.GSK3β调控EZH2影响乳腺癌干细胞的机制研究[D].武汉:华中科技大学,2016.
[11]吴秋英,吴小霞.Gsk-3β在卵巢浆液性肿瘤中的表达及意义[J].齐齐哈尔医学院学报,2015,36(10):1425-1426.
[12]CHEN S,HUANG L,SUN K,et al.Enhancer of zeste homolog 2as an independent prognostic marker for cancer:a meta-analysis[J].PLoS One,2015,10(5):e125480.
[13]陶丽,盛晓波,刘玉萍,等.GSK-3β活性调节与肿瘤治疗[J].中国药理学通报,2014,30(6):741-744.
[14]梁爽爽.子宫内膜癌组织中GSK-3β、WISP-1和Caspase-3的表达研究[D].广州:广州医学院,2012.
[2]SIEGEL R,MA J,ZOU Z,et al.Cancer statistics,2014[J].CA cancer J Clin,2014,64(1):9-29.
[3]SIEGEL R L,MILLER K D,JEMAL A.Cancer statistics,2015[J].CA Cancer J Clin,2015,65(1):5-29.
[4]SIEGEL R L,MILLER K D,JEMAL A.Cancer statistics,2016[J].CA Cancer J Clin,2016,66(1):7-30.
[5]DUZYJ C M,BUHIMSCHI I A,MOTAWEA H,et al.The invasive phenotype of placenta accreta extravillous trophoblasts associates with loss of E-cadherin[J].Placenta,2015,36(6):645-651.
[6]YAN D,AVTANSKI D,SAXENA N K,et al.Leptin-induced epithelial-mesenchymal transition in breast cancer cells requiresβ-catenin activation via Akt/GSK3-and MTal/Wnt1 protein-dependent pathways[J].J BiolChem,2012,287(11):8598-8612.
[7]SOKOLOSKY M,CHAPPELL W H,STADELMAN K,et al.Inhibition of GSK-3beta activity can result in drug and hormonal resistance and alter sensitivity to targeted therapy in MCF-7breast cancer cells[J].Cell Cycle,2014,13(5):820-833.
[8]马竹君,冯红超,宋宇峰,等.GSK-3β、E-cadherin、Cytokeratin在口腔鳞状细胞癌中的表达及意义[J].贵州医药,2016,40(4):354-357.
[9]侯新新,赵萌,张贵宇.PPAR7基因表达对子宫内膜癌细胞迁移、侵袭及增殖能力的影响[J].中华妇产科杂志,2014,49(5):360-365.
[10]胡福清.GSK3β调控EZH2影响乳腺癌干细胞的机制研究[D].武汉:华中科技大学,2016.
[11]吴秋英,吴小霞.Gsk-3β在卵巢浆液性肿瘤中的表达及意义[J].齐齐哈尔医学院学报,2015,36(10):1425-1426.
[12]CHEN S,HUANG L,SUN K,et al.Enhancer of zeste homolog 2as an independent prognostic marker for cancer:a meta-analysis[J].PLoS One,2015,10(5):e125480.
[13]陶丽,盛晓波,刘玉萍,等.GSK-3β活性调节与肿瘤治疗[J].中国药理学通报,2014,30(6):741-744.
[14]梁爽爽.子宫内膜癌组织中GSK-3β、WISP-1和Caspase-3的表达研究[D].广州:广州医学院,2012.