Bisphenol A-induced NF-κB activation enhances proliferation and migration of renal cell carcinoma cells via SLC7A11 upregulation and redox remodeling.

Bisphenol A (BPA) is a ubiquitous endocrine-disrupting chemical, yet its influence on renal cell carcinoma (RCC) remains unclear. We examined whether low-dose BPA alters redox regulation linked to ferroptosis susceptibility in 786-O and ACHN cells. After concentration screening, 100 nM BPA was used for mechanistic experiments. BPA enhanced proliferation and migration, increased the glutathione redox ratio (GSH/GSSG), reduced reactive oxygen species (ROS) signals, and preserved mitochondrial membrane potential. Public cancer dataset analyses prioritized SLC7A11, which was upregulated by BPA at mRNA and protein levels. Under inhibition of the cystine/glutamate antiporter system xc- with erastin, BPA co-treatment partially attenuated cytotoxicity and functional suppression. BPA increased NF-κB p65 phosphorylation, and pyrrolidine dithiocarbamate reduced p-p65 and SLC7A11 expression. These findings suggest that environmentally relevant BPA exposure may promote stress-tolerant phenotypes in RCC cells via an NF-κB-SLC7A11-associated antioxidant response.