Cellular senescence in vivo:: a barrier to tumorigenesis
Cellular senescence in vivo:: a barrier to tumorigenesis
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DOI：
10.1016/j.ceb.2008.01.007
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发表时间：
2008-04-01
影响因子：
7.5
通讯作者：
Peeper, Daniel S.
中科院分区：
文献类型：
--
作者：
Prieur, Alexandre;Peeper, Daniel S.
细胞衰老的特征在于细胞周期停滞，这在很大程度上是不可逆的，可以由许多类型的内在和外在应激触发。这些包括端粒功能障碍、癌基因激活和肿瘤抑制基因失活。最终，这些事件最终导致肿瘤抑制基因网络的激活。自从十多年前第一次描述癌基因诱导的细胞衰老（OIS）以来，许多后续研究已经证实OIS阻止细胞在体外进行致癌转化。然而，长期以来一直争论是否存在任何体内相关性。直到最近几年，才有越来越多的证据表明，体内OIS确实对应于对抗癌症的主要保护机制。在这篇评论中，我们强调了最近的一些发展。
Cellular senescence is characterized by a largely irreversible cell cycle arrest that can be triggered by many types of intrinsic and extrinsic stress. These include telomere malfunction, oncogene activation and tumor suppressor gene inactivation. Ultimately, such events culminate in the activation of a tumor suppressor gene network. Since the first description of Oncogene-Induced cellular Senescence (OIS) little over a decade ago, many subsequent studies have confirmed that OIS prevents cells from undergoing oncogenic transformation in vitro. However, it has long been debated whether any in vivo correlates exist. It is only since recent years that evidence has been accumulating indicating that OIS in vivo does correspond to a major protective mechanism against cancer. In this review, we highlight some of the recent developments.