Human EAG1 potassium channels in the epithelial-to-mesenchymal transition in lung cancer cells.

BACKGROUND Human ether à go-go-1 (EAG1) potassium channels are potential tools for cancer diagnosis, prognosis and therapy. Epithelial-to-mesenchymal transition (EMT) is a likely mechanism by which tumor cells become malignant. We wondered whether EAG1 is regulated in human lung tumor cells undergoing EMT. MATERIALS AND METHODS EMT was induced in A549 lung tumor cells with transforming growth factor beta (TGFβ1). EAG1 gene expression was assesed by real-time RT-PCR and protein expression by flow cytometry. RESULTS TGFβ1 produced the expected changes in morphology, migration and gene expression associated to EMT. EAG1 gene and protein expression were up-regulated during EMT. Astemizole did not prevent EMT. CONCLUSION Our results suggest that EAG1 channels participate in the acquisition of a malignant phenotype in lung tumor cells. Their potential role in EMT might not be uniquely related to their conducting function, in accordance with the reported tumor growth supported by non-conducting EAG1 channels.