Open AccessHormone-Like Effects of Bisphenol A on p53 and Estrogen Receptor Alpha in Breast Cancer Cells
Author(s) -
Victoria Lloyd,
Mia Morse,
Betsy Purakal,
Jordan Parker,
Paige Benard,
Michael Crone,
Samantha Pfiffner,
Monica Szmyd,
Sumi Dinda
Publication year - 2019
Publication title -
bioresearch open access
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.457
H-Index - 26
eISSN - 2164-7860
pISSN - 2164-7844
DOI - 10.1089/biores.2018.0048
Subject(s) - estrogen receptor , western blot , estrogen receptor alpha , bisphenol a , chemistry , estrogen , cell , gel electrophoresis , cell growth , receptor , cancer cell , blot , microbiology and biotechnology , cancer research , medicine , endocrinology , breast cancer , biology , cancer , biochemistry , organic chemistry , epoxy , gene
Bisphenol A (BPA) is a polymerizing agent commonly found in plastics that has been linked to xenoestrogenic activity. In this study, we analyzed the estrogen-like effects of BPA on the expression of estrogen receptor (ER)α and p53 with hormonal and antihormonal treatments in T-47D and MCF-7 cells. Cells were cultured in medium containing 5% charcoal-stripped fetal bovine serum for 6 days to deplete any endogenous steroids or effectors. The cells were then treated for 24 h with 600 nM BPA, which was determined to be the optimal value by a concentration study of BPA from 1 nM to 2 μM. Extracted cellular proteins were quantified and subjected to sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE)/Western blot analysis. The cell proliferation assays were quantified upon exposure to BPA. Laser confocal microscopy was performed to determine the cytolocalization of p53 and ERα upon treatment with BPA. Western blot analysis revealed that BPA caused an increase in the cellular protein p53 in a concentration-dependent manner. While treatment with BPA did not affect the cytolocalization of p53, an increase in cell proliferation was observed. Our studies provide interesting leads to delineate the possible mechanistic relationship among BPA, ER, and tumor suppressor proteins in breast cancer cells.