Delayed and persistent ERK1/2 activation is required for 4-hydroxytamoxifen-induced cell death

文献类型： 外文期刊

第一作者： Zhou, Jian-Hua

作者： Zhou, Jian-Hua;Yu, David V.;Cheng, Jingwei;Shapiro, David J.

作者机构：

关键词： tamoxifen;apoptosis;ERK;estrogen receptor

期刊名称：STEROIDS （ 影响因子：2.668； 五年影响因子：2.692 ）

ISSN： 0039-128X

年卷期： 2007 年 72 卷 11-12 期

页码：

收录情况： SCI

摘要： Tamoxifen (Tam), and its active metabolite, 4-hydroxytamoxifen (OHT), compete with estrogens for binding to the estrogen receptor (ER). Tam and OHT can also induce ER-dependent apoptosis of cancer cells. 10-100 nM OHT induces ER-dependent apoptosis in similar to 3 days. Using HeLaER6 cells, we examined the role of OHT activation of signal transduction pathways in OHT-ER-mediated apoptosis. OHT-ER activated the p38, JNK and ERK1/2 pathways. Inhibition of p38 activation with SB203580, or RNAi-knockdown of p38 alpha, moderately reduced OHT-ER mediated cell death. A JNK inhibitor partly reduced cell death. Surprisingly, the MEK1/2 inhibitor, PD98059, completely blocked OHT-ER induced apoptosis. EGF, an ERK1/2 activator, enhanced OHT-induced apoptosis. OHT induced a delayed and persistent phosphorylation of ERK1/2 that persisted for > 80 h. Addition of PD98059 as late as 24 h after OHT largely blocked OHT-ER mediated apoptosis. The antagonist, ICI 182,780, blocked both the long-term OHT-mediated phosphorylation of ERK1/2 and OHT-induced apoptosis. Our data suggests that the p38 and JNK pathways, which often play a central role in apoptosis, have only a limited role in OHT-ER-mediated cell death. Although rapid activation of the ERK1/2 pathway is often associated with cell growth, persistent activation of the ERK1/2 pathway is essential for OHT-ER induced cell death. (c) 2007 Elsevier Inc. All rights reserved.

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