Histone deacetylase 3 represses p15INK4b and p21WAF1/cip1 transcription by interacting with Sp1

被引：40

作者：

Huang, WF ^{[1
]}

Tan, DP ^{[1
]}

Wang, XL ^{[1
]}

Han, SY ^{[1
]}

Tan, J ^{[1
]}

Zhao, YM ^{[1
]}

Lu, J ^{[1
]}

Huang, BQ ^{[1
]}

机构：

[1] NE Normal Univ, Inst Cytol & Genet, Changchun 130024, Peoples R China

来源：

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 2006年 / 339卷 / 01期

基金：

中国国家自然科学基金;

关键词：

HDAC3; Sp1; repression; p15(INK4b); p21(WAF1/cip1); cell cycle;

D O I：

10.1016/j.bbrc.2005.11.010

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：

Histone deacetylase 3 (HDAC3) has been implicated to play roles in governing cell proliferation. Here we demonstrated that the over-expression of HDAC3 repressed transcription of p15(INK4b) and p21(WAF1/cip1) genes in 293T cells, and that the recruitment of HDAC3 to the promoter regions of these genes was critical to this repression. We also showed that HDAC3 repressed GAL4-Sp1 transcriptional activity, and that Sp1 was co-immunopreciptated with FLAG-tagged HDAC3. We conclude that HDAC3 can repress p15(INK4b) and p21(WAF1/cip1) transcription by interacting with Sp1. Furthermore, knockdown of HDAC3 by RNAi up-regulated the transcriptional expression of p15(INK4b), but not that of p21(WAF1/cip1), implicating the different roles of HDAC3 in repression of p15(INK4b) and p21(WAF1/cip1) transcription. Data from this study indicate that the inhibition of p15(INK4b) and p21(WAF1/cip1) may be one of the mechanisms by which HDAC3 participates in cell cycle regulation and oncogenesis. (c) 2005 Elsevier Inc. All rights reserved.

引用

页码：165 / 171

页数：7

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