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Loss of epithelial polarity and gain in invasiveness by carcinoma cells are critical events in the aggressive progression of cancers and depend on phenotypic transition programs such as the epithelial-to-mesenchymal transition (EMT). Many studies have reported the aberrant expression of voltage-gated sodium channels (Na V ) in carcinomas and specifically the Na V 1.5 isoform, encoded by the  SCN5A  gene, in breast cancer. Na V 1.5 activity, through an entry of sodium ions, in breast cancer cells is associated with increased invasiveness, but its participation to the EMT has to be clarified. In this study, we show that reducing the expression of Na V 1.5 in highly aggressive human MDA-MB-231 breast cancer cells reverted the mesenchymal phenotype, reduced cancer cell invasiveness and the expression of the EMT-promoting transcription factor  SNAI1 . The heterologous expression of Na V 1.5 in weakly invasive MCF-7 breast cancer cells induced their expression of both  SNAI1  and  ZEB1  and increased their invasive capacities. In MCF-7 cells the stimulation with the EMT-activator signal TGF-β1 increased the expression of  SCN5A . Moreover, the reduction of the salt-inducible kinase 1 (SIK1) expression promoted Na V 1.5-dependent invasiveness and expression of EMT-associated transcription factor SNAI1. Altogether, these results indicated a prominent role of SIK1 in regulating Na V 1.5-dependent EMT and invasiveness.

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Sodium Channel Nav1.5 Controls Epithelial-to-Mesenchymal Transition and Invasiveness in Breast Cancer Cells Through its Regulation by the Salt-Inducible Kinase-1