miR-383 inhibits proliferation and induces apoptosis via targeting HDAC2 in non-small cell lung cancer cells

Lung cancer is the most common cause of deaths among all cancers around the world and non-small cell lung cancer (NSCLC) accounts for approximately 85% of all lung cancer cases. In this study, we investigated the expression level of miR-383 and its biological function in NSCLC. Firstly, we observed miR-383 down-regulation and HDAC2 up-regulation in NSCLC by qRT-PCR and Western blot, respectively. Next, we found that HDAC2 levels were inversely correlated with miR-383 expression in NSCLC tumor tissues and identified HDAC2 as a direct target of miR-383 by luciferase reporter assay. Then, the functional in vitro assays indicated that ectopic overexpression of miR-383 inhibited proliferation and induced apoptosis in NSCLC A549 cells, while restoration of HDAC2 partially attenuated these effects of miR-383 on A549 cells. In addition, knockdown of miR-383 resulted in an increase in proliferation and a decrease in apoptosis of A549 cells. In conclusion, our findings revealed the suppressive role of miR-383 in the development of NSCLC and suggested that miR-383 may serve as a useful diagnostic marker and a potential therapeutic target in human lung cancer.