Study on ovarian cancer cell migration induced by bisphenol A via the MAPK and PI3K signaling pathways

Abstract

Objective To explore the role of bisphenol A in ovarian cancer cell migration and its molecular mechanism. Methods The human OVCAR-3 ovarian cancer cell line was chosen as research materials in this study. The 8 μm pore size Boyden chambers and QMC Chemotaxis Cell Migration Assay were adopted for OVCAR-3 cell migration analysis. The molecules involved in cell migration were measured by real-time fluorescent quantitative PCR, western blot and SensoLyte 490 Assay kits. The molecular mechanism of cell migration induced by bisphenol A was studied by the inhibition of ERK1/2 and PI3K molecules using their corresponding inhibitors. Results After 24 h incubation with bisphenol A (40 nM and 100 nM) , the OVCAR-3 cell migration was markedly enhanced (P<0.001) . Not only were the gene and protein expression levels of MMP-2, MMP-9 and N-calcium were significantly increased (P<0.05, P<0.01 or P<0.001) by bisphenol A, but also the activities of MMP-2 and MMP-9 were obviously enhanced (P<0.01) , indicating these three molecules were engaged in the cell migration caused by bisphenol A. Upon the inhibition of ERK1/2 or PI3K, the OVCAR-3 cell migration invoked by bisphenol A was offset, and the protein expression levels of MMP-2, MMP-9 and N-calcium as well as the activities of MMP-2 and MMP-9 were decreased. Conclusion The role of bisphenol A in ovarian cancer cell migration was achieved via ERK1/2 and PI3K signaling pathways. Key words: Bisphenol A; Ovarian cancer; MAPK; PI3K; Cell migration