Transcriptional regulation of cellular senescence

被引：74

作者：

Lanigan, F. ^{[1
]}

Geraghty, J. G. ^{[3
]}

Bracken, A. P. ^{[1
,2
]}

机构：

[1] Trinity Coll Dublin, Smurfit Genet Dept, Smurfit Inst Genet, Dublin 2, Ireland

[2] Natl Childrens Hosp, Adelaide & Meath Hosp, Dublin, Ireland

[3] Univ Coll Dublin, St Vincents Hosp, Dept Breast & Endocrine Surg, Dublin 2, Ireland

来源：

ONCOGENE | 2011年 / 30卷 / 26期

基金：

爱尔兰科学基金会;

关键词：

cellular senescence; transcription; cancer therapy; ONCOGENE-INDUCED SENESCENCE; INK4A TUMOR-SUPPRESSOR; DEMETHYLASE JMJD3 CONTRIBUTES; INDUCED PREMATURE SENESCENCE; E2F TARGET GENES; HISTONE DEACETYLASE; RETINOBLASTOMA PROTEIN; HUMAN FIBROBLASTS; CANCER-THERAPY; IN-VIVO;

D O I：

10.1038/onc.2011.34

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Cellular senescence is an irreversible arrest of proliferation. It is activated when a cell encounters stress such as DNA damage, telomere shortening or oncogene activation. Like apoptosis, it impedes tumour progression and acts as a barrier that pre-neoplastic cells must overcome during their evolution toward the full tumourigenic state. This review focuses on the role of transcriptional regulators in the control of cellular senescence, explores how their function is perturbed in cancer and discusses the potential to harness this knowledge for future cancer therapies. Oncogene (2011) 30, 2901-2911; doi:10.1038/onc.2011.34; published online 7 March 2011

引用

页码：2901 / 2911

页数：11

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