Maintaining cell identity: PRC2-mediated regulation of transcription and cancer

被引：337

作者：

Comet, Itys ^{[1
,2
]}

Riising, Eva M. ^{[4
]}

Leblanc, Benjamin ^{[1
,2
,3
]}

Helin, Kristian ^{[1
,2
,3
]}

机构：

[1] Univ Copenhagen, BRIC, Ole Maaloes Vej 5, DK-2200 Copenhagen, Denmark

[2] Univ Copenhagen, Ctr Epigenet, Ole Maaloes Vej 5, DK-2200 Copenhagen, Denmark

[3] Univ Copenhagen, Fac Hlth & Med Sci, Danish Stem Cell Ctr Danstem, Blegdamsvej 3, DK-2200 Copenhagen, Denmark

[4] Francis Crick Inst, 1 Midland Rd, London NW1 1AT, England

来源：

NATURE REVIEWS CANCER | 2016年 / 16卷 / 12期

基金：

欧盟第七框架计划; 新加坡国家研究基金会; 英国医学研究理事会; 欧洲研究理事会;

关键词：

REPRESSIVE COMPLEX 2; HISTONE METHYLTRANSFERASE EZH2; POLYCOMB GROUP PROTEINS; EPITHELIAL-MESENCHYMAL TRANSITION; SOMATIC MUTATIONS; STEM-CELLS; GENE EZH2; DEVELOPMENTAL REGULATORS; MYELODYSPLASTIC SYNDROME; SELECTIVE-INHIBITION;

D O I：

10.1038/nrc.2016.83

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

Enhancer of zeste homologue 2 (EZH2), the catalytic subunit of Polycomb repressive complex 2 (PRC2), has attracted broad research attention in the past few years because of its involvement in the development and maintenance of many types of cancer and the use of specific EZH2 inhibitors in clinical trials. Several observations show that PRC2 can have both oncogenic and tumour-suppressive functions. We propose that these apparently opposing roles of PRC2 in cancer are a consequence of the molecular function of the complex in maintaining, rather than specifying, the transcriptional repression state of its several thousand target genes.

引用

页码：803 / 810

页数：8

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