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Background  Na V 1.5 voltage-gated sodium channels are abnormally expressed in breast tumours and their expression level is associated with metastatic occurrence and patients’ death. In breast cancer cells, Na V 1.5 activity promotes the proteolytic degradation of the extracellular matrix and enhances cell invasiveness.    Findings  In this study, we showed that the extinction of Na V 1.5 expression in human breast cancer cells almost completely abrogated lung colonisation in immunodepressed mice (NMRI nude). Furthermore, we demonstrated that ranolazine (50 μM) inhibited Na V 1.5 currents in breast cancer cells and reduced Na V 1.5-related cancer cell invasiveness  in vitro. In vivo , the injection of ranolazine (50 mg/kg/day) significantly reduced lung colonisation by Na V 1.5-expressing human breast cancer cells.    Conclusions  Taken together, our results demonstrate the importance of Na V 1.5 in the metastatic colonisation of organs by breast cancer cells and indicate that small molecules interfering with Na V  activity, such as ranolazine, may represent powerful pharmacological tools to inhibit metastatic development and improve cancer treatments.    Electronic supplementary material  The online version of this article (doi:10.1186/1476-4598-13-264) contains supplementary material, which is available to authorized users.

Ranolazine inhibits NaV1.5-mediated breast cancer cell invasiveness and lung colonization