Treatment with Bisphenol A Leads to the Promotion of Human Breast Cancer Cells and Alteration of Cell Cycle-Related Gene Expressions, cyclin E and p27

Abstract

Endocrine disrupting chemicals (EDCs) have detrimental effects on human health. Among these EDCs, bisphenol A (BPA) binds to the estrogen receptors (ERs) to stimulate estrogen-mediated responses. BPA is assumed to disrupt reproductive and development system on human. In addition, BPA has been suspected as a risk of carcinogenesis recently. Because BPA can cause abnormal estrogen-mediated response in the organism, the exposure to BPA may stimulate the growth of estrogen-dependent breast cancers in human. In breast cancer, cyclin E and cyclin-dependent kinase inhibitor p27 are important in G1/S phase transition during the cell cycle progression. In this study, we investigated the effect of BPA on the proliferation of MCF-7 breast cancer cells in vitro using an MTT assay. Also, we analyzed the transcriptional levels of cyclin E and p27 following BPA treatment using semi-quantitative RT-PCR. As a result, BPA significantly induced the breast cancer cell growth compared to a vehicle. BPA caused the alterations of cyclin E and p27 mRNA expressions. The expression of cyclin E was increased by BPA, while p27 was decreased at 24 h after treatment of BPA in MCF-7 breast cancer cells. Taken together, these collective results suggest that the exposure of BPA induced breast cancer cell proliferation with deregulation of cell cycle. A further study is required to determine effects of BPA on carcinogenic process in in vivo models.