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

共 23 条

[1] Comparative application of antibody and gene array for expression profiling in human squamous cell lung carcinoma [J].

Bartling, B ;

Hofmann, HS ;

Boettger, T ;

Hansen, G ;

Burdach, S ;

Silber, RE ;

Simm, A .

LUNG CANCER, 2005, 49 (02) :145-154

[2] Differential display cloning of a novel human histone deacetylase (HDAC3) cDNA from PHA-activated immune cells [J].

Dangond, F ;

Hafler, DA ;

Tong, JK ;

Randall, J ;

Kojima, R ;

Utku, N ;

Gullans, SR .

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 1998, 242 (03) :648-652

[3]

Doetzlhofer A, 1999, MOL CELL BIOL, V19, P5504

[4] Nuclear accumulation of p21Cip1 the onset of mitosis:: a role at the G2/M-phase transition [J].

Dulic, V ;

Stein, GH ;

Far, DF ;

Reed, SI .

MOLECULAR AND CELLULAR BIOLOGY, 1998, 18 (01) :546-557

[5] Role of Class I and Class II histone deacetylases in carcinoma cells using siRNA [J].

Glaser, KB ;

Li, JL ;

Staver, MJ ;

Wei, RQ ;

Albert, DH ;

Davidsen, SK .

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 2003, 310 (02) :529-536

[6] Role for BRG1 in cell cycle control and tumor suppression [J].

Hendricks, KB ;

Shanahan, F ;

Lees, E .

MOLECULAR AND CELLULAR BIOLOGY, 2004, 24 (01) :362-376

[7] p15INK4b in HDAC inhibitor-induced growth arrest [J].

Hitomi, T ;

Matsuzaki, Y ;

Yokota, T ;

Takaoka, Y ;

Sakai, T .

FEBS LETTERS, 2003, 554 (03) :347-350

[8] The N-CoR/histone deacetylase 3 complex is required for repression by thyroid hormone receptor [J].

Ishizuka, T ;

Lazar, MA .

MOLECULAR AND CELLULAR BIOLOGY, 2003, 23 (15) :5122-5131

[9] BRG1 controls the activity of the retinoblastoma protein via regulation of p21CIP1/WAF1/SDI [J].

Kang, H ;

Cui, KR ;

Zhao, KJ .

MOLECULAR AND CELLULAR BIOLOGY, 2004, 24 (03) :1188-1199

[10] Histone acetylases and deacetylases in cell proliferation [J].

Kouzarides, T .

CURRENT OPINION IN GENETICS & DEVELOPMENT, 1999, 9 (01) :40-48

← 1 2 3 →