MiR-32 Suppresses the Development of Lung Cancer via Modulating PI3K/Akt

Abstract

Our team utilized qRT-PCR for prospecting miR-32 expression level in primary lung carcinoma tissues and cell lines, as well as Kaplan–Meier method for dissecting the relation of miR-32 expression with the prognosis of lung carcinoma. We transfected lung cancer A549 cells with miR-32 mimic/inhibitor and mimic/inhibitor NC, and appraised the influences of miR-32 on the phenotype changes of lung carcinoma cells via MTT assay, wound healing assay and cell apoptosis assay, separately. Then the target gene of miR-32 was predicted via bioinformatics. Finally, Western blotting was adopted for analyzing the impact of alteration of miR-32 expression on the PI3K/Akt axis in A549 cells. In lung carcinoma tissues as well as cells, miR-32 expression is down-regulated, and miR-32 partakes in the progress of lung carcinoma via PI3K/Akt pathway.