MicroRNA-363-3p inhibits cell growth and invasion of non-small cell lung cancer by targeting HMGA2

Abstract

Lung cancer is the second most common cancer and is the leading cause of cancer-related death worldwide. For decades, increasing evidence revealed that microRNAs may contribute to non-small cell lung cancer (NSCLC) carcinogenesis and progression and could provide novel therapeutic targets for treatments of patients with NSCLC. Accumulated studies indicate that microRNA (miR)-363-3p serves important roles in tumorigenesis and tumor development; however, the role of miR-363-3p in NSCLC is still unclear. The current study reported that miR-363-3p exhibited reduced expression in NSCLC tissues and cell lines. Reduced miR-363-3p expression was correlated with tumor node metastasis classification and distant metastasis of NSCLC patients. Notably, miR-363-3p re-expression significantly suppressed cell proliferation and invasion of NSCLC. Furthermore, bioinformatics analysis, luciferase reporter assay, reverse transcription-quantitative polymerase chain reaction and western blotting indicated that (high mobility group AT-hook 2) HMGA2 was a direct target gene of miR-363-3p. HMGA2 was increased in NSCLC tissues and inversely associated with HMGA2 expression. Moreover, HMGA2 underexpression had similar effects to miR-363-3p overexpression in NSCLC cells. Thus, the current study suggested that miR-363-3p may act as a tumor suppressor in NSCLC and that the miR-363-3p could be investigated as a therapeutic target for the patients with this disease.