Bisphenol A triggers the malignancy of nasopharyngeal carcinoma cells via activation of Wnt/beta-catenin pathway.

It is critical to understand the risk factors responsible for the tumorigenesis and progression of nasopharyngeal carcinoma (NPC). Bisphenol A (BPA) can regulate the estrogenic signals to modulate cancer progression, while its roles in NC were not investigated. Our present study revealed that the BPA can increase proliferation and migration of NPC cells while decrease the chemosensitivity to doxorubicin (Dox). The inhibitor of GSK-3beta/beta-catenin (LiCl) can restore BPA-induced cell proliferation of NPC cells, which is due to that BPA can decrease phosphorylation while increase expression and nucleus localization of beta-catenin. Mechanistically, BPA can increase the mRNA stability of beta-catenin (encoded by CTNNB1) via suppressing the expression of miR-214-3p, which can direct target the 3'UTR of beta-catenin mRNA. Further, BPA can decrease phosphorylation of beta-catenin via repressing the expression of CK1alpha. Collectively, our data showed that BPA can trigger the proliferation and malignancy of NPC cells via activation of Wnt/beta-catenin pathway. It indicated that body accumulation and inhalation exposure of BPA might be a risk factor for NPC development.