Abstract Title:

Bisphenol A Increases the Migration and Invasion of Triple Negative Breast Cancer Cells via Oestrogen-related Receptor Gamma.

Abstract Source:

Basic Clin Pharmacol Toxicol. 2016 Apr 2. Epub 2016 Apr 2. PMID: 27038254

Abstract Author(s):

Xiao-Lin Zhang, Na Liu, Shan-Fan Weng, Hong-Sheng Wang

Article Affiliation:

Xiao-Lin Zhang


Triple-negative breast cancer (TNBC) is characterized by great metastasis and invasion capability. Our present study revealed that nanomolar bisphenol A (BPA), one of the most ubiquitous endocrine disruptors, can increase wound closure and invasion of both MDA-MB-231 and BT-549 cells. BPA treatment can increase protein and mRNA expression of matrix metalloprotease 2 (MMP-2) and MMP-9, while had no effect on the expression of vimentin (Vim) and fibronectin (FN) in TNBC cells. The expression of G protein-coupled receptor (GPER), which has been suggested to mediate rapid oestrogenic signals, was not varied in BPA-treated MDA-MB-231 and BT-549 cells. Its inhibitor G15 also had no effect on BPA-induced MMPs expression and cell invasion. Interestingly, BPA treatment can significantly increase the mRNA and protein expression of oestrogen-related receptorγ (ERRγ), but not ERRα or ERRβ, in both MDA-MB-231 and BT-549 cells. The knock-down of ERRγ can markedly attenuate BPA-induced expression of MMP-2 and MMP-9 in TNBC cells. BPA treatment can activate both ERK1/2 and Akt in TNBC cells. Both inhibitors of ERK1/2 (PD98059) and Akt (LY294002) can attenuate BPA-induced ERRγ expression and cell invasion of MDA-MB-231 cells. Collectively, our data revealed that BPA can increase the expression of MMPs and in vitro motility of TNBC cells via ERRγ. Both activation of ERK1/2 and Akt participated in this process. Our study suggests that more attention should be paid to the roles of xenoestrogens such as BPA in the development and progression of TNBC. This article is protected by copyright. All rights reserved.

Study Type : In Vitro Study
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Adverse Pharmacological Actions : Proliferative : CK(17) : AC(0)

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