GSE171150
Potassium channel-driven bioelectric signaling affects the metastatic potential of triple negative breast cancer
Our data demonstrate that altering the RMP of triple-negative breast cancer (TNBC) cells by manipulating potassium channels increases in vitro invasion, tumor growth, and metastasis, inducing changes in gene expression associated with cell adhesion. We describe a novel mechanism for RMP-mediated cell migration involving cadherin-11 and the MAPK pathway. Importantly, we identify a new treatment strategy for metastatic TNBC by repurposing FDA-approved potassium channel blockers. Our results provide an understanding of a mechanism by which the bioelectricity regulates cancer cell invasion and metastasis that can advance the development of a potential new class of TNBC therapeutics. Overall design: Examination of genetic changes in MDA-MB-231 human breast cancer cell line with overexpression of two different potassium ion channels, Kir2.1 and Kv1.5