Sedivy John M
Department of Molecular Biology, Cell Biology, and Biochemistry, Brown University, 70 Ship Street, Providence, RI 02903, USA.
Cancer Cell. 2007 May;11(5):389-91. doi: 10.1016/j.ccr.2007.04.014.
Cellular senescence triggered by telomere dysfunction has long been hypothesized to constitute a tumor suppression mechanism. The evidence has come primarily from in vitro cell culture studies, and more indirectly from analysis of tumor specimens. Two recent studies, published in the current issue of Cancer Cell and online at EMBO Reports, provide direct mechanistic evidence in cleverly manipulated mouse cancer models. This work shows that telomere-induced senescence is as effective as apoptosis in reducing cancer incidence and is mediated by the tumor suppressor p53.
长期以来,人们一直假设由端粒功能障碍引发的细胞衰老构成一种肿瘤抑制机制。证据主要来自体外细胞培养研究,以及对肿瘤标本的间接分析。最近发表在本期《癌细胞》以及在线发表于《EMBO报告》上的两项研究,在巧妙构建的小鼠癌症模型中提供了直接的机制证据。这项工作表明,端粒诱导的衰老在降低癌症发病率方面与细胞凋亡同样有效,并且由肿瘤抑制因子p53介导。