Bisphenol A Effects on Estrogen Receptor β Expression: Implications in Prostate Cancer

Janet K. Hess-Wilson, Shuk-Mei Ho, Ph.D. and Karen E. Knudsen, Ph.D.
University of Cincinnati College of Medicine
NIEHS Grants T32ES007250 and P30ES006096

Bisphenol A causes down regulation of gene expression for estrogen receptor β (ERβ) and likely regulates cell proliferation in prostate cancer according to new research from NIEHS grantees at the University of Cincinnati. 

Prostate adenocarcinomas are dependent on the androgen receptor for growth and progression.  Current therapies are aimed at repressing androgen receptor activity; however, androgen receptor activity can be reactivated through somatic mutations that form mutant receptors.  These altered receptors can be activated by alternative ligands including bisphenol A, an endocrine disrupting chemical that is found in many plastics.

Using a prostate cancer cell line containing mutant androgen receptors and employing DNA microarray analysis, the researchers were able to show that bisphenol A dramatically reduced ERβ expresson. Since ERβ functions to antagonize the androgen receptor function and androgen receptor-dependent cell proliferation, decreasing its expression could likely lead to growth of prostate tumors.  Future research in this laboratory will focus on the contribution of ERβ on the bisphenol A-induced proliferative response.

Citation: Hess-Wilson JK, Webb SL, Daly HK, Leung YK, Boldison J, Comstock CE, Sartor MA, Ho SM, Knudsen KE. Unique bisphenol A transcriptome in prostate cancer: novel effects on ERbeta expression that correspond to androgen receptor mutation status. Environ Health Perspect. 2007 Nov;115(11):1646-53.