Aneuploidy and cancer
Aneuploidy and cancer
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DOI：
10.1002/jcb.21484
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发表时间：
2007-10-15
影响因子：
4
通讯作者：
Jeang, Kuan-Teh
中科院分区：
文献类型：
--
作者：
Chi, Ya-Hui;Jeang, Kuan-Teh
细胞的整倍体状态受其他机制的影响，包括完整的纺锤体组装检查点(SAC)、准确的中心体周期和适当的细胞质分裂。在哺乳动物细胞中的研究表明，SAC功能失调、中心体周期和胞质分裂都可以显著促进非整倍体。有趣的是，人类癌症通常是非整倍体的，并且在SAC基因中表现出表达的变化。SAC是一个多蛋白质复合体，监测姐妹染色单体的错误分离。最近的几个实验小鼠模型表明，SAC减弱与体内肿瘤发生之间存在联系。在这里，我们简要回顾了一些导致细胞非整倍性的机制，并对非整倍体与人类癌症的关系提供了一个展望。
The cell's euploid status is influenced by, amongst other mechanisms, an intact spindle assembly checkpoint (SAC), an accurate centrosome cycle, and proper cytokinesis. Studies in mammalian cells suggest that dysregulated SAC function, centrosome cycle, and cytokinesis can all contribute significantly to aneuploidy. Of interest, human cancers are frequently aneuploid and show altered expression in SAC genes. The SAC is a multi-protein complex that monitors against mis-segregation of sister chromatids. Several recent experimental mouse models have suggested a link between weakened SAC and in vivo tumorigenesis. Here, we review in brief some mechanisms which contribute to cellular aneuploicly and offer a perspective on the relationship between aneuploidy and human cancers.