内复制及其在肿瘤发生发展中的作用
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摘要
大多数的二倍体细胞通常通过G1期(DNA合成前期)、S期(DNA合成期)、G2期(DNA合成后期)和M期(分裂期)经典细胞周期完成细胞增殖。然而,在动、植物中也广泛存在着一种与有丝分裂不同的细胞周期过程,即内复制。在内复制过程中,G期和S期交替出现,细胞并不发生分裂,导致产生多倍体细胞。内复制在人体的正常发育、器官形成、创伤愈合过程中必不可少。近年来,越来越多的研究关注内复制与肿瘤发生、演进的关系。本文就内复制的生理作用做一概述,并讨论内复制在肿瘤发生、发展中的可能作用及相关分子机制。
Most diploid cells proliferate by proceeding through the canonical G1(DNA pre-synthesis), S(DNA synthesis), G2(DNA postsynthesis), and M(mitosis) phases of the cell cycle. However, there is another type of cell cycle that occurs frequently in both plants and animals, known as endoreplication. Endoreplication consists of alternating periods of G and S phases without cytokinesis, which results in polyploidy. It is indispensable for normal development, organ formation, and wound healing in humans. In recent years, considerable attention has been paid to delineating the connections of endoreplication with tumorigenesis and tumor progression. Here,we review the role of endoreplication in normal human development and discuss its possible role in tumor development and the underlying molecular mechanisms.
Most diploid cells proliferate by proceeding through the canonical G1(DNA pre-synthesis), S(DNA synthesis), G2(DNA postsynthesis), and M(mitosis) phases of the cell cycle. However, there is another type of cell cycle that occurs frequently in both plants and animals, known as endoreplication. Endoreplication consists of alternating periods of G and S phases without cytokinesis, which results in polyploidy. It is indispensable for normal development, organ formation, and wound healing in humans. In recent years, considerable attention has been paid to delineating the connections of endoreplication with tumorigenesis and tumor progression. Here,we review the role of endoreplication in normal human development and discuss its possible role in tumor development and the underlying molecular mechanisms.
引文
[1]Fox DT, Duronio RJ. Endoreplication and polyploidy:insights into development and disease[J]. Development, 2013, 140(1):3-12.
[2]Zielke N, Edgar BA, DePamphilis ML. Endoreplication[J]. Cold Spring Harb Perspect Biol, 2013, 5(1):a012948.
[3]Gandarillas A, Molinuevo R, Sanz-Gomez N. Mammalian endoreplication emerges to reveal a potential developmental timer[J]. Cell Death Differ, 2018, 25(3):471-476.
[4]Shu Z, Row S, Deng WM. Endoreplication:The Good, the Bad, and the Ugly[J]. Trends Cell Biol, 2018, 28(6):465-474.
[5]Edgar BA, Zielke N, Gutierrez C. Endocycles:a recurrent evolutionary innovation for post-mitotic cell growth[J]. Nat Rev Mol Cell Biol,2014,15(3):197-210.
[6]Storchova Z, Pellman D. From polyploidy to aneuploidy, genome instability and cancer[J]. Nat Rev Mol Cell Biol, 2004, 5(1):45-54.
[7]Unhavaithaya Y, Orr-Weaver TL. Polyploidization of glia in neural development links tissue growth to blood-brain barrier integrity[J].Genes Dev, 2012, 26(1):31-36.
[8]Athayde Wirka K, Chen AA, Conaghan J, et al. Atypical embryo phenotypes identified by time-lapse microscopy:high prevalence and association with embryo development[J]. Fertil Steril, 2014, 101(6):1637-1648.
[9]Iwata K, Yumoto K, Sugishima M, et al. Analysis of compaction initiation in human embryos by using time-lapse cinematography[J]. J Assist Reprod Genet, 2014, 31(4):421-426.
[10]Ravid K, Lu J, Zimmet JM, et al. Roads to polyploidy:the megakaryocyte example[J]. J Cell Physiol, 2002, 190(1):7-20.
[11]Tamori Y, Deng WM. Tissue repair through cell competition and compensatory cellular hypertrophy in postmitotic epithelia[J]. Dev Cell, 2013, 25(4):350-363.
[12]Losick VP, Fox DT, Spradling AC. Polyploidization and cell fusion contribute to wound healing in the adult Drosophila epithelium[J]. Curr Biol, 2013, 23(22):2224-2232.
[13]Xiang J, Bandura J, Zhang P, et al. EGFR-dependent TOR-independent endocycles support Drosophila gut epithelial regeneration[J]. Nat Commun, 2017, 8:15125.
[14]Diril MK, Ratnacaram CK, Padmakumar VC, et al. Cyclin-dependent kinase 1(Cdk1)is essential for cell division and suppression of DNA rereplication but not for liver regeneration[J]. Proc Natl Acad Sci U S A,2012, 109(10):3826-3831.
[15]Pandit SK, Westendorp B, Nantasanti S, et al. E2F8 is essential for polyploidization in mammalian cells[J]. Nat Cell Biol, 2012, 14(11):1181-1191.
[16]Weigmann K, Cohen SM, Lehner CF. Cell cycle progression, growth and patterning in imaginal discs despite inhibition of cell division after inactivation of Drosophila Cdc2 kinase[J]. Development, 1997, 124(18):3555-3563.
[17]Follette PJ, Duronio RJ, O'Farrell PH. Fluctuations in cyclin E levels are required for multiple rounds of endocycle S phase in Drosophila[J].Curr Biol, 1998, 8(4):235-238.
[18]Spradling AC. Germline cysts:communes that work[J]. Cell. 1993, 72(5):649-651.
[19]Artavanis-Tsakonas S, Rand MD, Lake RJ. Notch signaling:cell fate control and signal integration in development[J]. Science, 1999, 284(5415):770-776.
[20]Deng WM, Althauser C, Ruohola-Baker H. Notch-Delta signaling induces a transition from mitotic cell cycle to endocycle in Drosophila follicle cells[J]. Development, 2001, 128(23):4737-4746.
[21]Schaeffer V, Althauser C, Shcherbata HR, et al. Notch-dependent Fizzyrelated/Hec1/Cdh1 expression is required for the mitotic-to-endocycle transition in Drosophila follicle cells[J]. Curr Biol, 2004, 14(7):630-636.
[22]Cong B, Ohsawa S, Igaki T. JNK and Yorkie drive tumor progression by generating polyploid giant cells in Drosophila[J]. Oncogene, 2018, 37(23):3088-3097.
[23]Duncan AW, Hanlon Newell AE, Smith L, et al. Frequent aneuploidy among normal human hepatocytes[J]. Gastroenterology, 2012, 142(1):25-28.
[24]Zhang B, Mehrotra S, Ng WL, et al. Low levels of p53 protein and chromatin silencing of p53 target genes repress apoptosis in Drosophila endocycling cells[J]. PLoS Genet, 2014, 10(9):e1004581.
[25]Mosieniak G, Sliwinska MA, Alster O, et al. Polyploidy Formation in Doxorubicin-Treated Cancer Cells Can Favor Escape from Senescence[J]. Neoplasia, 2015, 17(12):882-893.
[26]Chen S, Stout JR, Dharmaiah S, et al. Transient endoreplication downregulates the kinesin-14 HSET and contributes to genomic instability[J]. Mol Biol Cell, 2016, 27(19):2911-2923.
[27]Niu N, Mercado-Uribe I, Liu J. Dedifferentiation into blastomere-like cancer stem cells via formation of polyploid giant cancer cells[J].Oncogene, 2017, 36(34):4887-4900.
[28]Zhang S, Mercado-Uribe I, Liu J. Generation of erythroid cells from fibroblasts and cancer cells in vitro and in vivo[J]. Cancer Lett, 2013,333(2):205-212.
[29]Laughney AM, Elizalde S, Genovese G, et al. Dynamics of Tumor Heterogeneity Derived from Clonal Karyotypic Evolution[J]. Cell Rep, 2015,12(5):809-820.
[30]Chen J, Niu N, Zhang J, et al. Polyploid Giant Cancer Cells(PGCCs):The Evil Roots of Cancer[J]. Curr Cancer Drug Targets, 2018.[Epub ahead of print]
[31]Zhang D, Yang X, Yang Z, et al. Daughter Cells and Erythroid Cells Budding from PGCCs and Their Clinicopathological Significances in Colorectal Cancer[J]. J Cancer, 2017, 8(3):469-478.
[32]Liu J. The Dualistic Origin of Human Tumors[J]. Semin Cancer Biol, 2018.[Epub ahead of print]
[2]Zielke N, Edgar BA, DePamphilis ML. Endoreplication[J]. Cold Spring Harb Perspect Biol, 2013, 5(1):a012948.
[3]Gandarillas A, Molinuevo R, Sanz-Gomez N. Mammalian endoreplication emerges to reveal a potential developmental timer[J]. Cell Death Differ, 2018, 25(3):471-476.
[4]Shu Z, Row S, Deng WM. Endoreplication:The Good, the Bad, and the Ugly[J]. Trends Cell Biol, 2018, 28(6):465-474.
[5]Edgar BA, Zielke N, Gutierrez C. Endocycles:a recurrent evolutionary innovation for post-mitotic cell growth[J]. Nat Rev Mol Cell Biol,2014,15(3):197-210.
[6]Storchova Z, Pellman D. From polyploidy to aneuploidy, genome instability and cancer[J]. Nat Rev Mol Cell Biol, 2004, 5(1):45-54.
[7]Unhavaithaya Y, Orr-Weaver TL. Polyploidization of glia in neural development links tissue growth to blood-brain barrier integrity[J].Genes Dev, 2012, 26(1):31-36.
[8]Athayde Wirka K, Chen AA, Conaghan J, et al. Atypical embryo phenotypes identified by time-lapse microscopy:high prevalence and association with embryo development[J]. Fertil Steril, 2014, 101(6):1637-1648.
[9]Iwata K, Yumoto K, Sugishima M, et al. Analysis of compaction initiation in human embryos by using time-lapse cinematography[J]. J Assist Reprod Genet, 2014, 31(4):421-426.
[10]Ravid K, Lu J, Zimmet JM, et al. Roads to polyploidy:the megakaryocyte example[J]. J Cell Physiol, 2002, 190(1):7-20.
[11]Tamori Y, Deng WM. Tissue repair through cell competition and compensatory cellular hypertrophy in postmitotic epithelia[J]. Dev Cell, 2013, 25(4):350-363.
[12]Losick VP, Fox DT, Spradling AC. Polyploidization and cell fusion contribute to wound healing in the adult Drosophila epithelium[J]. Curr Biol, 2013, 23(22):2224-2232.
[13]Xiang J, Bandura J, Zhang P, et al. EGFR-dependent TOR-independent endocycles support Drosophila gut epithelial regeneration[J]. Nat Commun, 2017, 8:15125.
[14]Diril MK, Ratnacaram CK, Padmakumar VC, et al. Cyclin-dependent kinase 1(Cdk1)is essential for cell division and suppression of DNA rereplication but not for liver regeneration[J]. Proc Natl Acad Sci U S A,2012, 109(10):3826-3831.
[15]Pandit SK, Westendorp B, Nantasanti S, et al. E2F8 is essential for polyploidization in mammalian cells[J]. Nat Cell Biol, 2012, 14(11):1181-1191.
[16]Weigmann K, Cohen SM, Lehner CF. Cell cycle progression, growth and patterning in imaginal discs despite inhibition of cell division after inactivation of Drosophila Cdc2 kinase[J]. Development, 1997, 124(18):3555-3563.
[17]Follette PJ, Duronio RJ, O'Farrell PH. Fluctuations in cyclin E levels are required for multiple rounds of endocycle S phase in Drosophila[J].Curr Biol, 1998, 8(4):235-238.
[18]Spradling AC. Germline cysts:communes that work[J]. Cell. 1993, 72(5):649-651.
[19]Artavanis-Tsakonas S, Rand MD, Lake RJ. Notch signaling:cell fate control and signal integration in development[J]. Science, 1999, 284(5415):770-776.
[20]Deng WM, Althauser C, Ruohola-Baker H. Notch-Delta signaling induces a transition from mitotic cell cycle to endocycle in Drosophila follicle cells[J]. Development, 2001, 128(23):4737-4746.
[21]Schaeffer V, Althauser C, Shcherbata HR, et al. Notch-dependent Fizzyrelated/Hec1/Cdh1 expression is required for the mitotic-to-endocycle transition in Drosophila follicle cells[J]. Curr Biol, 2004, 14(7):630-636.
[22]Cong B, Ohsawa S, Igaki T. JNK and Yorkie drive tumor progression by generating polyploid giant cells in Drosophila[J]. Oncogene, 2018, 37(23):3088-3097.
[23]Duncan AW, Hanlon Newell AE, Smith L, et al. Frequent aneuploidy among normal human hepatocytes[J]. Gastroenterology, 2012, 142(1):25-28.
[24]Zhang B, Mehrotra S, Ng WL, et al. Low levels of p53 protein and chromatin silencing of p53 target genes repress apoptosis in Drosophila endocycling cells[J]. PLoS Genet, 2014, 10(9):e1004581.
[25]Mosieniak G, Sliwinska MA, Alster O, et al. Polyploidy Formation in Doxorubicin-Treated Cancer Cells Can Favor Escape from Senescence[J]. Neoplasia, 2015, 17(12):882-893.
[26]Chen S, Stout JR, Dharmaiah S, et al. Transient endoreplication downregulates the kinesin-14 HSET and contributes to genomic instability[J]. Mol Biol Cell, 2016, 27(19):2911-2923.
[27]Niu N, Mercado-Uribe I, Liu J. Dedifferentiation into blastomere-like cancer stem cells via formation of polyploid giant cancer cells[J].Oncogene, 2017, 36(34):4887-4900.
[28]Zhang S, Mercado-Uribe I, Liu J. Generation of erythroid cells from fibroblasts and cancer cells in vitro and in vivo[J]. Cancer Lett, 2013,333(2):205-212.
[29]Laughney AM, Elizalde S, Genovese G, et al. Dynamics of Tumor Heterogeneity Derived from Clonal Karyotypic Evolution[J]. Cell Rep, 2015,12(5):809-820.
[30]Chen J, Niu N, Zhang J, et al. Polyploid Giant Cancer Cells(PGCCs):The Evil Roots of Cancer[J]. Curr Cancer Drug Targets, 2018.[Epub ahead of print]
[31]Zhang D, Yang X, Yang Z, et al. Daughter Cells and Erythroid Cells Budding from PGCCs and Their Clinicopathological Significances in Colorectal Cancer[J]. J Cancer, 2017, 8(3):469-478.
[32]Liu J. The Dualistic Origin of Human Tumors[J]. Semin Cancer Biol, 2018.[Epub ahead of print]
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