Transcriptional Regulation of the p16 Tumor Suppressor Gene

被引：4

作者：

Kotake, Yojiro ^{[1
]}

Naemura, Madoka ^{[1
]}

Murasaki, Chihiro ^{[1
]}

Inoue, Yasutoshi ^{[1
]}

Okamoto, Haruna ^{[1
]}

机构：

[1] Kinki Univ, Fac Humanity Oriented Sci & Engn, Dept Biol & Environm Chem, Iizuka, Fukuoka 8208555, Japan

来源：

ANTICANCER RESEARCH | 2015年 / 35卷 / 08期

关键词：

Cell cycle; CDK inhibitor; p16; transcription; polycomb; MLL; ANRIL; review; LONG NONCODING RNAS; DEMETHYLASE JMJD3 CONTRIBUTES; CELL-CYCLE CONTROL; HISTONE H3; INDUCED SENESCENCE; OVER-EXPRESSION; INK4A-ARF LOCUS; CDK INHIBITORS; ONCOGENIC RAS; POLYCOMB;

D O I：

暂无

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

The p16 tumor suppressor gene encodes a specific inhibitor of cyclin-dependent kinase (CDK) 4 and 6 and is found altered in a wide range of human cancers. p16 plays a pivotal role in tumor suppressor networks through inducing cellular senescence that acts as a barrier to cellular transformation by oncogenic signals. p16 protein is relatively stable and its expression is primary regulated by transcriptional control. Polycomb group (PcG) proteins associate with the p16 locus in a long non-coding RNA, ANRIL-dependent manner, leading to repression of p16 transcription. YB1, a transcription factor, also represses the p16 transcription through direct association with its promoter region. Conversely, the transcription factors Ets1/2 and histone H3K4 methyltransferase MLL1 directly bind to the p16 locus and mediate p16 induction during replicative and premature senescence. In the present review, we discuss the molecular mechanisms by which these factors regulate p16 transcription.

引用

页码：4397 / 4401

页数：5