HDAC3 regulates stability of estrogen receptor α mRNA

被引:15
|
作者
Oie, Shohei
Matsuzaki, Kazuya
Yokoyama, Wataru
Murayama, Akiko
Yanagisawa, Junn [1 ]
机构
[1] Univ Tsukuba, Grad Sch Life & Environm Sci, Tsukuba, Ibaraki 3058577, Japan
[2] Univ Tsukuba, Ctr Tsukuba Adv Res Alliance, Tsukuba, Ibaraki 3058577, Japan
基金
日本科学技术振兴机构; 日本学术振兴会;
关键词
ER alpha; Breast cancer; HDAC inhibitor; HDAC3; mRNA stability; Cell proliferation; BREAST-CANCER CELLS; DEACETYLASE INHIBITOR TRICHOSTATIN; GENE-EXPRESSION; HUR; CARCINOMA; DEGRADATION; RECRUITMENT; PROGRESSION; TAMOXIFEN; PROMOTER;
D O I
10.1016/j.bbrc.2013.02.007
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
Estrogen receptor alpha (ER alpha) expression is a risk factor for breast cancer. HDAC inhibitors have been demonstrated to down-regulate ER alpha expression in ER alpha-positive breast cancer cell lines, but the molecular mechanisms are poorly understood. Here, we showed that HDAC inhibitors decrease the stability of ER alpha mRNA, and that knockdown of HDAC3 decreases the stability of ER alpha mRNA and suppresses estrogen-dependent proliferation of ER alpha-positive MCF-7 breast cancer cells. In the Oncomine database, expression levels of HDAC3 in ER alpha-positive tumors are higher than those in ER alpha-negative tumors, thus suggesting that HDAC3 is necessary for ER alpha mRNA stability, and is involved in the estrogen-dependent proliferation of ER alpha-positive tumors. Crown Copyright (C) 2013 Published by Elsevier Inc. All rights reserved.
引用
收藏
页码:236 / 241
页数:6
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