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Oncol Lett. 2017 Sep;14(3):2635-2642. doi: 10.3892/ol.2017.6469. Epub 2017 Jun 23.

Effects of low dose of bisphenol A on the proliferation and mechanism of primary cultured prostate epithelial cells in rodents.

Huang D1,2,3, Wu J2,3, Su X2,3, Yan H2,3, Sun Z2,3.

Author information

1
School of Pharmacy, Fudan University, Shanghai 200433, P.R. China.
2
National Evaluation Centre for The Toxicology of Fertility Regulating Drugs, Shanghai Institute of Planned Parenthood Research, Shanghai 200032, P.R. China.
3
National Population and Family Planning Key Laboratory of Contraceptive Drugs and Devices, Shanghai Institute of Planned Parenthood Research, Shanghai 200032, P.R. China.

Abstract

Bisphenol A (BPA) is a well-known endocrine disruptor compound (EDC) that aggravates testosterone-induced benign prostate hyperplasia by increasing the relative weight of the ventral and dorsolateral prostate in rats. This phenomenon is primarily attributed to the exogenous estrogen effect of BPA. However, the direct effect of BPA on prostate cells has not been characterized. The present study investigated the proliferative effect and possible mechanisms of action of BPA on the prostatic epithelium of rats. The ventral prostate epithelial cells were cultured in vitro and the proliferation effects of BPA on cells were studied. The cells were identified as prostatic epithelial cells, and cell viability, cell apoptosis and the expressions of androgen receptors (AR) and estrogen receptors (ER), were detected. It was observed that 0.01-1 nM BPA promoted cell growth, with 1 nM BPA inducing the greatest increase in the rate of cell growth. However, BPA-treated cells exhibited no marked morphological changes compared with the control group. The cell apoptosis rate in each BPA-treated group was lower compared with the control group. The expression levels of ERα and ERβ increased, but the expression of AR decreased. The present study demonstrated that environmental exposure to BPA directly promoted the proliferation of prostate cells in rats through increasing the expression of estrogen receptors, reducing the expression of androgen receptors of the cells and decreasing apoptosis-induced cell death.

KEYWORDS:

bisphenol A; environmental estrogen; epithelial cell; in vitro; primary culture; prostate

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