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p53 抑制肿瘤形成:使细胞衰老。

Tumor suppression by p53: making cells senescent.

机构信息

Center for Comparative Oncology, University of California, Davis, California 95616, USA.

出版信息

Histol Histopathol. 2010 Apr;25(4):515-26. doi: 10.14670/HH-25.515.

DOI:10.14670/HH-25.515
PMID:20183804
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2841029/
Abstract

Cellular senescence is a permanent cell cycle arrest and a potent tumor suppression mechanism. The p53 tumor suppressor is a sequence-specific transcription factor and acts as a central hub sensing various stress signals and activating an array of target genes to induce cell cycle arrest, apoptosis, and senescence. Recent reports showed that restoration of p53 induces premature senescence and tumor regression in mice with hepatocarcinomas or sarcomas. Thus, p53-mediated senescence is capable of eliminating cancer cells in vivo. p63 and p73, two homologues of p53, have similar function in cell cycle arrest and apoptosis. However, the role of p63 and p73 in cellular senescence is elusive. In this review, we will discuss how p53 regulates senescence and future studies about p53 family members in senescence.

摘要

细胞衰老(Cellular senescence)是一种永久性的细胞周期停滞,也是一种强大的肿瘤抑制机制。p53 肿瘤抑制因子是一种序列特异性转录因子,作为一个中央枢纽,能够感知各种应激信号,并激活一系列靶基因,从而诱导细胞周期停滞、细胞凋亡和衰老。最近的报告显示,在患有肝癌或肉瘤的小鼠中,恢复 p53 可诱导过早衰老和肿瘤消退。因此,p53 介导的衰老能够在体内消除癌细胞。p63 和 p73 是 p53 的两个同源物,在细胞周期停滞和细胞凋亡方面具有相似的功能。然而,p63 和 p73 在细胞衰老中的作用尚不清楚。在这篇综述中,我们将讨论 p53 如何调节衰老,以及关于 p53 家族成员在衰老中的未来研究。

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Tumor suppression by p53: making cells senescent.p53 抑制肿瘤形成:使细胞衰老。
Histol Histopathol. 2010 Apr;25(4):515-26. doi: 10.14670/HH-25.515.
2
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本文引用的文献

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TAp73 knockout shows genomic instability with infertility and tumor suppressor functions.TAp73基因敲除显示出基因组不稳定,并伴有不育和肿瘤抑制功能。
Genes Dev. 2008 Oct 1;22(19):2677-91. doi: 10.1101/gad.1695308. Epub 2008 Sep 19.
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Ras oncogenes: split personalities.Ras癌基因:具有双重特性。
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ID1, inhibitor of differentiation/DNA binding, is an effector of the p53-dependent DNA damage response pathway.ID1(分化/DNA结合抑制剂)是p53依赖性DNA损伤反应途径的效应器。
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ATR signaling can drive cells into senescence in the absence of DNA breaks.在没有DNA断裂的情况下,ATR信号传导可促使细胞进入衰老状态。
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DEC1, a basic helix-loop-helix transcription factor and a novel target gene of the p53 family, mediates p53-dependent premature senescence.DEC1是一种碱性螺旋-环-螺旋转录因子,也是p53家族的一个新靶基因,介导p53依赖的早衰。
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