MicroRNA-520c enhances cell proliferation, migration, and invasion by suppressing IRF2 in gastric cancer.

Dysregulation of microRNA (miRNA) is actively involved in the development and progression of gastric cancer (GC). MiR-520c was previously found to be overexpressed in GC specimens and cells. However, the clinical significance of miR-520c and its biological function in GC remain largely unknown. Here, we found that miR-520c expression in GC tissues was significantly increased compared to normal adjacent gastric tissues. Its increased level was prominently correlated with poor clinical parameters and prognosis of GC patients. Accordingly, the expression of miR-520c was obviously elevated in GC cell lines as compared with gastric epithelial cells. Overexpression of miR-520c in N-87 cells significantly increased the proliferative ability, migration, and invasion of cancer cells, while miR-520c silencing suppressed MKN-45 cell proliferation, migration, and invasion in vitro. Mechanically, miR-520c inversely regulated interferon regulatory factor 2 (IRF2) abundance in GC cells. Herein, IRF2 was found to be a downstream target of miR-520c in GC. Furthermore, IRF2 was down-regulated in GC tissues compared to nontumor tissues. An inverse correlation between IRF2 and miR-520c expression was observed in GC cases. Taken together, miR-520c may serve as a prognostic predictor and a therapeutic target for GC patients.