Non-canonical functions of the RB protein in cancer

被引:126
|
作者
Dick, Frederick A. [1 ,2 ]
Goodrich, David W. [3 ]
Sage, Julien [4 ,5 ]
Dyson, Nicholas J. [6 ]
机构
[1] Western Univ, Childrens Hlth Res Inst, London Reg Canc Program, London, ON, Canada
[2] Western Univ, Dept Biochem, London Reg Canc Program, London, ON, Canada
[3] Roswell Pk Canc Inst, Dept Pharmacol & Therapeut, Buffalo, NY 14263 USA
[4] Stanford Univ, Dept Pediat, Stanford, CA 94305 USA
[5] Stanford Univ, Dept Genet, Stanford, CA 94305 USA
[6] Harvard Med Sch, Lab Mol Oncol, Ctr Canc, Massachusetts Gen Hosp, Charlestown, MA USA
基金
美国国家卫生研究院; 加拿大健康研究院;
关键词
RETINOBLASTOMA TUMOR-SUPPRESSOR; CELL LUNG-CANCER; NEUROENDOCRINE PROSTATE-CANCER; E2F1-SPECIFIC BINDING DOMAIN; DOUBLE-STRAND BREAKS; DNA-DAMAGE; CYCLE CONTROL; THERAPEUTIC RESPONSE; GROWTH-FACTOR; STEM-CELLS;
D O I
10.1038/s41568-018-0008-5
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
The canonical model of RB-mediated tumour suppression developed over the past 30 years is based on the regulation of E2F transcription factors to restrict cell cycle progression. Several additional functions have been proposed for RB, on the basis of which a non-canonical RB pathway can be described. Mechanistically, the non-canonical RB pathway promotes histone modification and regulates chromosome structure in a manner distinct from cell cycle regulation. These functions have implications for chemotherapy response and resistance to targeted anticancer agents. This Opinion offers a framework to guide future studies of RB in basic and clinical research.
引用
收藏
页码:442 / 451
页数:10
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