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.