期刊
CELL REPORTS
卷 19, 期 12, 页码 2423-2431出版社
CELL PRESS
DOI: 10.1016/j.celrep.2017.05.055
关键词
-
类别
资金
- Marie Curie Initial Training Network Project PLOIDYNET [607722, FP7-PEOPLE-2013]
- Gravitation Program (Cancer Genomics Center, CGC.nl) [58588]
- Dutch Cancer Foundation [NKI-2015-7832]
The presence of an abnormal karyotype has been shown to be profoundly detrimental at the cellular and organismal levels but is an overt hallmark of cancer. Aneuploidy can lead to p53 activation and thereby prevents proliferation, but the exact trigger for p53 activation has remained controversial. Here, we have used a system to induce aneuploidy in untransformed human cells to explore how cells deal with different segregation errors. We show that p53 is activated only in a subset of the cells with altered chromosome content. Importantly, we find that at least a subset of whole-chromosome aneuploidies can be propagated in p53-proficient cells, indicating that aneuploidy does not always lead to activation of p53. Finally, we demonstrate that propagation of structural aneuploidies (gain or loss of part of a chromosome) induced by segregation errors is limited to p53-deficient cells.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据