p15INK4b in HDAC inhibitor-induced growth arrest

被引：66

作者：

Hitomi, T ^{[1
]}

Matsuzaki, Y ^{[1
]}

Yokota, T ^{[1
]}

Takaoka, Y ^{[1
]}

Sakai, T ^{[1
]}

机构：

[1] Kyoto Prefectural Univ Med, Grad Sch Med Sci, Dept Mol Targeting Canc Prevent, Kamigyo Ku, Kyoto 6028566, Japan

来源：

FEBS LETTERS | 2003年 / 554卷 / 03期

关键词：

p15(INK4b); HDAC inhibitor; trichostatin A; butyrate; G1; arrest; promoter; p21(WAF1/Cip1);

D O I：

10.1016/S0014-5793(03)01186-4

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 (HDAC) inhibitors arrest human tumor cells at the G1 phase of the cell cycle and activate the cyclin-dependent kinase inhibitor, p21(WAF1/Cip1). However, several studies have suggested the existence of a p21(WAF1/Cip1)-independent molecular pathway. We report here that HDAC inhibitors, trichostatin A (TSA) and sodium butyrate, activate the p15(INK4b) gene, a member of the INK4 gene family, through its promoter in HaCaT cells. Furthermore, we show that up-regulation of p15(INK4b) by TSA is associated with cell growth inhibition of HCT116 p21 (-/-) cells. Our findings suggest that p15(INK4b) is one of the important molecular targets of HDAC inhibitors. (C) 2003 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.

引用

页码：347 / 350

页数：4

共 27 条

[1]

[Anonymous], 1983, COLD SPRING HARBOR L

[2] p21WAF1 is required for butyrate-mediated growth inhibition of human colon cancer cells [J].