Abstract
Lung cancer is the leading cause of cancer-associated mortality worldwide. MicroRNAs (miRNAs/miRs) serve a role in the occurrence and development of lung cancer. The aim of the present study was to analyze the expression and function of the proliferation-associated miR-383-5p in lung adenocarcinoma (LAC). Samples of human LAC and matched adjacent normal lung tissues were surgically removed, and miR-383-5p expression and the pathological characteristics of lung adenocarcinoma were investigated. The present study revealed that miR-383-5p expression level was significantly decreased in LAC tissues and its expression levels were markedly associated with tumor size and differentiation. Overexpression of miR-383-5p in A549 and H1299 LAC cell lines inhibited cell proliferation by G1 cell cycle phase arrest and induction of apoptosis. Cancerous inhibitor of protein phosphatase 2A (CIP2A), a potential target gene of miR-383-5p, was inversely associated with miR-383-5p expression level in LAC tissues and cell lines. Furthermore, the results of the present study demonstrated that CIP2A was directly regulated by miR-383-5p and the restoration of CIP2A expression reversed the inhibitory effects of miR-383-5p on LAC cell proliferation. In conclusion, the results of the present study demonstrated that miR-383-5p was downregulated in LAC tissues. By targeting CIP2A, miR-383-5p exerts its anti-proliferative function in LAC, suggesting its use a potential novel potential prognostic biomarker and therapeutic target for LAC.