MicroRNA-139-5p suppresses non-small cell lung cancer progression by targeting ATAD2.

MiR-139-5p is a suppressor in multiple types of cancer. However, whether miR-139-5p affects NSCLC is unknown. In this study, miR-139-5p expression in clinical samples was examined by real-time PCR and in situ hybridization (ISH). MiR-139-5p mimic was transfected to monitor NSCLC cell behaviors. Potential target was predicated using bioinformatics database. Next, whether miR-139-5p impacted cell behaviors via regulation of its predicted target gene were further evaluated. The result revealed that miR-139-5p was lower in NSCLC samples/cells. MiR-139-5p restrained A549 cell proliferation, accelerated apoptosis, and inhibited the β-catenin signaling. ATAD2 was a predicted target of miR-139-5p, and it was highly expressed in NSCLC tissues. ATAD2 overexpression abolished the miR-139-5p's anti-tumor effect on cell proliferation and apoptosis. TWS119 (a β-catenin signaling activator) partially reversed miR-139-5p overexpression-induced suppression of cell proliferation and promotion of cell apoptosis. In tumor xenografts, miR-139-5p restrained tumor growth. MiR-139-5p was a tumor suppressor in NSCLC by regulating the oncogene ATAD2 and β-catenin signaling. Our study provides a promising target for cancer treatment.