Bisphenol A and ovarian cancer: emerging evidence and potential biological mechanisms

Abstract

This review summarizes current evidence concerning the relationship between bisphenol A (BPA) exposure and ovarian cancer (OC). Human epidemiological studies have mainly examined possible associations between BPA concentrations and OC occurrence, but their cross-sectional or case–control designs do not establish that BPA exposure increases OC risk. Experimental studies in OC cell lines and tumor-bearing animals suggest that BPA may alter tumor-related phenotypes, including proliferation, migration, invasion, angiogenesis, and stemness. These findings concern potential tumor progression rather than patient prognosis. Separate studies in normal ovarian tissue and granulosa cells indicate possible ovarian toxicity, including oxidative stress, apoptosis, and steroidogenic disturbances, but these findings should not be interpreted as direct evidence of OC risk. Mechanistically, BPA exposure has been reported to be associated with changes in endocrine signaling, oxidative processes, metabolism, and epigenetic regulation in selected experimental models. Overall, evidence linking BPA exposure to ovarian-cancer-related outcomes remains limited, and current findings do not establish that BPA causes OC or worsens patient prognosis in humans.