MicroRNA-652 inhibits proliferation and induces apoptosis of non-small cell lung cancer A549 cells

Increasing evidence suggests the down-regulation of microRNA-652 (miR-652) in various diseases, addressing its involvement in tumorigenesis, but its role in non-small cell lung cancer (NSCLC) is largely unexplored. This study therefore aims to uncover the function of miR-652 in regulating lung cancer cells. Human NSCLC A549 cells were transfected with the mimic or inhibitor of miR-652 to change miR-652 levels. MTT, 5-Bromo-2-deoxyuridine (BrdU), flow cytometry assays were performed to assess viability, proliferation and apoptosis of the transfected cells. Expression of p27, p21 and apoptotic factors including B-cell lymphoma 2 (BCL2), BCL2 associated X protein (BAX) and caspase 3 were examined by Western blot. Result showed that, miR-652 mimic inhibited, while miR-652 inhibitor increased A549 cell viability on the second and third days post transfection (P < 0.05). BrdU staining suggested that cell proliferative ability was suppressed by miR-652 mimic (P < 0.001) and induced by the inhibitor (P < 0.05). Expression of p21 appeared to be unaffected, whereas p27 was increased by miR-652, which was consistent with cell proliferative changes. Percent of apoptotic cells was increased by miR-652 mimic and reduced by the inhibitor (P < 0.01). Western blot further showed that miR-652 mimic decreased BCL2/BAX but elevated the proportion of cleaved caspase 3, and miR-652 inhibitor induced the opposite changes (P < 0.001). In conclusion, these results addressed the anti-proliferative and pro-apoptotic functions of miR-652 in A549 cells, providing a promising strategy for the molecular therapy of NSCLC.