Unravelling mechanisms of p53-mediated tumour suppression

被引：1079

作者：

Bieging, Kathryn T. ^{[1
]}

Mello, Stephano Spano ^{[1
]}

Attardi, Laura D. ^{[1
,2
]}

机构：

[1] Stanford Univ, Sch Med, Dept Radiat Oncol, Div Radiat & Canc Biol,CCSR South, Stanford, CA 94305 USA

[2] Stanford Univ, Sch Med, Dept Genet, CCSR South, Stanford, CA 94305 USA

来源：

NATURE REVIEWS CANCER | 2014年 / 14卷 / 05期

关键词：

CELL-CYCLE ARREST; DNA-DAMAGE RESPONSE; EPITHELIAL-MESENCHYMAL TRANSITION; MYC-INDUCED APOPTOSIS; MUTANT P53 GAIN; MOUSE MODELS; BREAST-CANCER; MICE LACKING; SPONTANEOUS TUMORIGENESIS; TRANSCRIPTIONAL CONTROL;

D O I：

10.1038/nrc3711

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

p53 is a crucial tumour suppressor that responds to diverse stress signals by orchestrating specific cellular responses, including transient cell cycle arrest, cellular senescence and apoptosis, which are all processes associated with tumour suppression. However, recent studies have challenged the relative importance of these canonical cellular responses for p53-mediated tumour suppression and have highlighted roles for p53 in modulating other cellular processes, including metabolism, stem cell maintenance, invasion and metastasis, as well as communication within the tumour microenvironment. In this Opinion article, we discuss the roles of classical p53 functions, as well as emerging p53-regulated processes, in tumour suppression.

引用

收藏

页码：359 / 370

页数：12

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