Bisphenol A induces a rapid activation of Erk1/2 through GPR30 in human breast cancer cells

被引:160
作者
Dong, S. [1 ,2 ]
Terasaka, S. [1 ]
Kiyama, R. [1 ]
机构
[1] Natl Inst Adv Ind Sci & Technol, Biomed Res Inst, Tsukuba, Ibaraki 3058566, Japan
[2] Chinese Acad Sci, Inst Urban Environm, Xiamen, Peoples R China
关键词
Bisphenol A; Erk1/2; Estrogen receptor; GPR30; Breast cancer cells; ESTROGEN-RECEPTOR-ALPHA; PROTEIN-COUPLED RECEPTOR; ENDOCRINE-DISRUPTING CHEMICALS; IN-VITRO; ENVIRONMENTAL ESTROGENS; C-FOS; G-PROTEIN-COUPLED-RECEPTOR-30; GPR30; LIQUID-CHROMATOGRAPHY; PRENATAL EXPOSURE; RISK-ASSESSMENT;
D O I
10.1016/j.envpol.2010.09.004
中图分类号
X [环境科学、安全科学];
学科分类号
08 ; 0830 ;
摘要
Bisphenol A (BPA) has been considered as an endocrine disruptor due to its ability to interact with estrogen receptors (ERs). While G protein-coupled receptor 30 (GPR30) is a novel estrogen receptor, its role in BPA-induced activation of Erk1/2 remains unknown. Human breast cancer cell lines, MCF-7, MDA-MB-231 and SKBR3, were used as experimental models to discriminate between ERs-dependent, putative ERs-independent and/or GPR30-associated effects. BPA induced a rapid activation of Erk1/2 in both ER alpha/beta-positive and negative breast cancer cells, and this effect was not blocked with an ER antagonist, ICI 182,780. A small interfering RNA assay revealed that the expression of GPR30 was necessary for BPA-induced activation of Erk1/2 and transcriptional regulation of c-fos. In addition, BPA regulates the expression of c-fos likely through an AP1-mediated pathway. As a conclusion, GPR30 plays an important role in the BPA-induced activation of Erk1/2 in a manner distinguishable from that in ER alpha-mediated signaling. (C) 2010 Elsevier Ltd. All rights reserved.
引用
收藏
页码:212 / 218
页数:7
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