Emerging roles of E2Fs in cancer: an exit from cell cycle control

被引：805

作者：

Chen, Hui-Zi ^{[1
,2
,3
]}

Tsai, Shih-Yin ^{[1
,2
]}

Leone, Gustavo ^{[1
,2
,3
]}

机构：

[1] Ohio State Univ, Human Canc Genet Program, Dept Mol Virol Immunol & Med Genet, Columbus, OH 43210 USA

[2] Ohio State Univ, Dept Mol Genet, Columbus, OH 43210 USA

[3] Ohio State Univ, Ctr Comprehens Canc, Coll Med & Publ Hlth, Integrated Med Sci Program, Columbus, OH 43210 USA

来源：

NATURE REVIEWS CANCER | 2009年 / 9卷 / 11期

基金：

美国国家卫生研究院;

关键词：

COMPARATIVE GENOMIC HYBRIDIZATION; TRANSCRIPTION FACTOR E2F-1; TRANSGENIC MOUSE MODEL; PROTEIN FAMILY-MEMBERS; LOSS-OF-HETEROZYGOSITY; HUMAN LUNG-CANCER; LENS FIBER CELLS; S-PHASE ENTRY; HEPATOCELLULAR-CARCINOMA; GENE-EXPRESSION;

D O I：

10.1038/nrc2696

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

Mutations of the retinoblastoma tumour suppressor gene (RB1) or components regulating the RB pathway have been identified in almost every human malignancy. The E2F transcription factors function in cell cycle control and are intimately regulated by RB. Studies of model organisms have revealed conserved functions for E2Fs during development, suggesting that the cancer-related proliferative roles of E2F family members represent a recent evolutionary adaptation. However, given that some human tumours have concurrent RB1 inactivation and E2F amplification and overexpression, we propose that there are alternative tumour-promoting activities for the E2F family, which are independent of cell cycle regulation.

引用

页码：785 / 797

页数：13

共 215 条

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