Overexpression and silencing experiments were conducted to confirm detected trends in PEMF and DOX sensitivities related to endogenous TRPC1 channel expression as well as to investigate the propensity of the resultant breast cancer cells to undergo epithelial-mesenchymal transition (EMT) that would provide clinical relevance to the heightened sensitivities to PEMFs and DOX conferred by TRPC1. This evidence concerns the gene TRPC1 and breast carcinoma.