Aberrant hypomethylation and overexpression of the eyes absent homologue 2 suppresses tumor cell growth of human lung adenocarcinoma cells.

The eyes absent homologue 2 (EYA2) is a dual-functional transcription factor/phosphatase that plays a critical role in neoplasia. The precise effects of EYA2 remain elusive in non-small cell lung cancer (NSCLC). In the present study, we examined EYA2 expression in NSCLC cell lines and a normal pulmonary epithelial cell line. We found that EYA2 was aberrantly upregulated in the lung adenocarcinoma cells. Therefore, we studied the methylation status of the eya2 gene in a lung adenocarcinoma cell line, a normal pulmonary epithelial cell line and lung adenocarcinoma tissues. Furthermore, the eya2 gene was knocked down in lung adenocarcinoma cells via RNA interference to investigate the regulatory role of EYA2; specifically, cell proliferation, cell cycle distribution, apoptosis, migration and invasive capacities were assessed in tje EYA2‑knockdown cancer cells. The results showed that the aberrant hypomethylation and overexpression of the eya2 gene were associated with lung adenocarcinoma oncogenesis. In addition, inhibition of EYA2 expression suppressed tumour cell growth by altering the proliferation, cell cycle distribution, apoptosis, migration and invasive capacities of the cells. These findings demonstrated that EYA2 functions as a stimulant in lung adenocarcinoma pathogenesis and may facilitate the development of novel diagnostic targets and therapy strategies for lung adenocarcinoma.