Overexpression of mir-489-3p inhibits proliferation and migration of non-small cell lung cancer cells by suppressing the HER2/PI3K/AKT/Snail signaling pathway

Background: Lung Cancer is a highly prevalent malignancy with significant morbidity and mortality rates. MiR-489-3p, a MicroRNA, has been identified as a regulator of tumor cell proliferation and invasion. Its expression is downregulated in non-small cell lung Cancer (NSCLC). Elucidating the molecular mechanisms underlying miR-489-3p's role in NSCLC pathogenesis is crucial for identifying potential diagnostic and therapeutic targets.

Methods: To investigate the molecular mechanism of miR-489-3p in NSCLC, this study utilized A549, a commonly used NSCLC cell line. MiR-489-3p mimics and inhibitors were transfected into A549 cells. Additionally, co-transfection experiments using wortmannin, an inhibitor of the PI3K/Akt pathway, were performed. Expression of miR-489-3p and related proteins was analyzed by Western blotting and quantitative Real-Time PCR (qRT-PCR). Cell migration and proliferation were assessed by wound healing and colony formation assays, respectively.

Results: Overexpression of miR-489-3p significantly inhibited the proliferation and migration of A549 cells. This inhibitory effect was further enhanced upon co-transfected with wortmannin. Analysis of human lung specimens showed increased expression of HER2, PI3K, and Akt in lung adenocarcinoma tissues compared to adjacent non-cancerous tissues.

Conclusions: These findings suggest that miR-489-3p overexpression may inhibit NSCLC cell proliferation and migration by suppressing the HER2/PI3K/Akt/Snail signaling pathway. This study elucidates miR-489-3p's molecular mechanisms in NSCLC and provides experimental basis for identifying early diagnostic markers and novel therapeutic targets.

HER2; Migration; Non-small cell lung cancer; Proliferation; miR-489–3p.