Lee Hyunsook
Department of Biological Sciences and the Institute of Molecular Biology and Genetics, Seoul National University, Seoul 151-742, Korea.
Mol Cells. 2014 Oct 31;37(10):713-8. doi: 10.14348/molcells.2014.0233. Epub 2014 Sep 26.
Alteration in chromosome numbers and structures instigate and foster massive genetic instability. As Boveri has seen a hundred years ago (Boveri, 1914; 2008), aneuploidy is hallmark of many cancers. However, whether aneuploidy is the cause or the result of cancer is still at debate. The molecular mechanism behind aneuploidy includes the chromo-some mis-segregation in mitosis by the compromise of spindle assembly checkpoint (SAC). SAC is an elaborate network of proteins, which monitor that all chromosomes are bipolarly attached with the spindles. Therefore, the weakening of the SAC is the major reason for chromosome number instability, while complete compromise of SAC results in detrimental death, exemplified in natural abortion in embryonic stage. Here, I will review on the recent progress on the understanding of chromosome mis-segregation and cancer, based on the comparison of different mouse models of BubR1, the core component of SAC.
染色体数量和结构的改变引发并加剧了大规模的遗传不稳定性。正如博韦里在一百年前所见（博韦里，1914年；2008年），非整倍体是许多癌症的标志。然而，非整倍体是癌症的原因还是结果仍存在争议。非整倍体背后的分子机制包括有丝分裂过程中纺锤体组装检查点（SAC）功能受损导致的染色体错误分离。SAC是一个由蛋白质组成的复杂网络，它监测所有染色体是否双极附着于纺锤体。因此，SAC功能减弱是染色体数量不稳定的主要原因，而SAC完全受损则会导致有害的死亡，如胚胎期自然流产所示。在此，我将基于对SAC核心成分BubR1不同小鼠模型的比较，综述在理解染色体错误分离与癌症方面的最新进展。
