MicroRNA-217 alleviates development of non-small cell lung cancer by inhibiting AKT3 via PI3K pathway

OBJECTIVE: To explore the role of microRNA-217 in non-small cell lung cancer (NSCLC) and its underlying mechanism. PATIENTS AND METHODS: MicroRNA-217 expression in 48 NSCLC tissues and paracancerous tissues were detected by qRT-PCR (quantitative Real-time polymerase chain reaction). The relationship between microRNA-217 expression and prognosis of NSCLC patients was analyzed. Target gene of microRNA-217 was predicted by bioinformatics method and further verified by luciferase reporter gene assay. Cell proliferation, cell cycle and apoptosis were detected after altering microRNA-217 expression in NSCLC cells. The effect of microRNA-217 on regulating PI3K pathway was detected by Western blot. RESULTS: MicroRNA-217 was downregulated in NSCLC tissues than that of paracancerous tissues. Shorter overall survival (OS) was observed in NSCLC patients with lower expression of microRNA-217 than those with higher expression. Overexpressed microRNA-217 remarkably inhibited proliferation and cell cycle, whereas induced apoptosis of NSCLC cells. AKT3 was screened out to be the target gene of microRNA-217. Western blot results demonstrated that microRNA-217 upregulated AKT3 and PI3K pathway-related genes. CONCLUSIONS: Downregulated microRNA-217 promotes the occurrence and progression of NSCLC through upregulating AKT3 via PI3K pathway.