Bisphenol A enhanced cell migration through Kv3.4 in MCF7 cells

Abstract

Bisphenol A (BPA) is a well-known endocrine-disrupting chemical (EDC) that has been implicated in cancer development. However, the specific mechanisms of EDCs, including BPA, remain unclear. Voltage-gated potassium (Kv) channels have been closely related to cancer. In particular, Kv3.4 plays a role in cancer malignancy, including cell migration via the ERK and AKT signaling pathways. In this study, we investigated the mechanism of BPA in relation to Kv3.4 expression in human breast cancer MCF7 cells. BPA treatment significantly increased Kv3.4 expression at both the mRNA and protein levels and induced cell migration. Further analysis demonstrated that Kv3.4 is closely related to integrin (3 and integrin-regulated FAK signaling. However, BPA-induced cell migration and integrin-regulated FAK signaling were significantly abolished by Kv3.4 silencing. Therefore, we concluded that BPA is closely associated with cancer cell migration mediated by Kv3.4 via integrin-regulated FAK signaling. These findings provide novel insights into the role of BPA in cancer progression and suggest Kv3.4 as a potential therapeutic target for BPA-associated cell migration.