MicroRNA HSA-miR-125a-5p induces apoptosis by activating p53 in lung cancer cells

Abstract

ABSTRACTThe mature microRNA hsa-miR-125a-5p is derived from the 5′ end of pre-miR-125a. Although hsa-miR-125a-5p is dysregulated in some tumors, its specific roles in lung cancer cell apoptosis is still unknown. To study its function, the authors examined the effects of hsa-miR-125a-5p on apoptosis in lung cancer cells and investigated its probable regulatory mechanism. The authors showed that hsa-miR-125a-5p expression was lower in different lung cancer cell lines than in Human bronchial epithelial (HBE) cells by quantitative reverse transcriptase–polymerase chain reaction (qRT-PCR). In gain-of-function experiments, the authors found that hsa-miR-125a-5p suppressed proliferation and induced apoptosis in A549 cells by MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) and flow cytometry, respectively. In addition, wild-type p53 mRNA and protein expression was increased by hsa-miR-125a-5p overexpression. Moreover, blocking wild-type p53 attenuated the effect of hsa-miR-125a-5p on apoptosis. In loss-of-function experiments, wild-type p53 mRNA and protein expression was decreased by blocking hsa-miR-125a-5p. The effect of hsa-miR-125a-5p inhibitor on apoptosis was also weakened by blocking wild-type p53. Taken together, these data suggest that hsa-miR-125a-5p induces apoptosis via a p53-dependent pathway in human lung cancer cells. These results provide new insight into the roles of the miR-125a family in lung cancer.