Aberrant methylation of the Cx26 gene may be involved in the development of lung adenocarcinomas induced by N-nitrosobis(2-hydroxypropyl)amine in rats.

Our results suggest the inactivation of Cx26 (connexin 26) in lung cancer may be explained by promoter methylation.

Reciprocal positive regulation between Cx26 and PI3K/Akt pathway confers acquired gefitinib resistance in non-small-cell lung carcinoma cells by promoting epithelial mesenchymal transition via a gap-junctional communication-independent manner.

Decreased expression of CX26 was found in nonsmall cell lung cancer (NSCLC) tissues. Its internalization promoted proliferation, epithelialmesenchymal transition and migration and thus induced NSCLC via aberrant activation of the P53/MDM2 signaling pathway under hypoxic conditions.