Bisphenol A (BPA) is a monomer use in manufacturing a wide range of chemical products which include
epoxy resins and
polycarbonate. It has been reported that BPA increases the cell proliferation activity of human
breast cancer MCF-7 cells as well as 17-beta
estradiol (E2) and
diethylstilbestrol (DES). However, BPA induces target genes through ER-dependent and ER-independent manners which are different from the actions induced by E2. Therefore, BPA may be unique in
estrogen-dependent cell proliferation compared to other
endocrine disrupting chemicals (EDCs). In the present study, to test whether
ERalpha is essential to the BPA-induced proliferation on MCF-7 cells, we suppressed the
ERalpha expression of MCF-7 cells by RNA interference (RNAi). Proliferation effects in the presence of E2, DES and BPA were not observed in
ERalpha-knockdown MCF-7 cells in comparison with control MCF-7. In addition, a marker of proliferative potential, MIB-1 labeling index (LI), showed no change in BPA-treated groups compared with vehicle-treated groups on
ERalpha-knockdown MCF-7 cells. In conclusion, we demonstrated that
ERalpha has a role in BPA-induced cell proliferation as well as E2 and DES. Moreover, this study indicated that the direct knockdown of
ERalpha using RNAi serves as an additional tool to evaluate, in parallel with MCF-7 cell proliferation assay, for potential EDCs.