Bisphenol A (BPA) is a widely used industrial chemical present in numerous consumer products such as plastics, epoxy resins, and thermal paper. Growing evidence suggests that BPA may pose potential health risks, particularly in relation to carcinogenesis. In this study, we investigated the toxic effects and carcinogenic role of BPA using two bladder cancer cell lines, T24 and UMUC. Our results show that BPA influences cell viability and migration in a dose-dependent manner. At low concentrations, BPA significantly promoted cell growth and cell migration in both T24 and UMUC cells, whereas higher concentrations suppressed cell growth. Proteomic and transcriptomic analyses further revealed substantial changes in protein and gene expression profiles following BPA exposure. Bioinformatics analysis suggested that BPA may modulate bladder cancer cell behavior through the MAPK signaling and inflammatory response pathways. Together, these findings offer important insights into the molecular mechanisms of BPA-induced cellular alterations, with potential implications for developing more targeted and effective therapeutic strategies for cancer. Future studies should focus on further elucidating the signaling pathways affected by BPA, exploring its potential synergistic or antagonistic interactions with other environmental factors, and validating these results through in vivo models.
Wang et al. (Wed,) studied this question.