Mitotic catastrophe and endomitosis in tumour cells: An evolutionary key to a molecular solution

被引:87
作者
Erenpreisa, J
Kalejs, M
Cragg, MS
机构
[1] Latvian State Univ, Lab Tum Cell Biol, Biomed Ctr, LV-1067 Riga, Latvia
[2] Univ Southampton, Southampton, Hants, England
[3] WEHI, Melbourne, Vic, Australia
关键词
mitotic catastrophe; tumours; endomitosis; somatic reduction; meiotic regulators;
D O I
10.1016/j.cellbi.2005.10.005
中图分类号
Q2 [细胞生物学];
学科分类号
071009 [细胞生物学]; 090102 [作物遗传育种];
摘要
Following genotoxic insult, p53 mutated tumour cells undergo mitotic catastrophe. This is characterised by a switch from mitosis to the endocycle. The essential difference between mitosis and the endocycle is that in the latter, DNA synthesis is uncoupled from cell division, which leads to the formation of endopolyploid cells. Recent data suggests that a return from the endocycle into mitosis is also possible. Furthermore, our observations indicate that a particular type of endocycle known as endomitosis may be involved in this return. Here we review the role of endomitosis in the somatic reduction of polyploidy during development and its postulated role in the evolution of meiosis. Finally, we incorporate these evolutionary data to help interpret our most recent observations in the tumour cell system, which indicate a role for endomitosis and meiotic regulators, in particular p39mos in the segregation of genomes (somatic reduction) of these endopolyploid cells. (c) 2005 International Federation for Cell Biology. Published by Elsevier Ltd. All rights reserved.
引用
收藏
页码:1012 / 1018
页数:7
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