MiR-873-5P controls gastric cancer progression by targeting hedgehog-GLI signaling

Gastric cancer is one of the most common human malignancies. Thus, it is important to explore the specific mechanism in which gastric cancer is induced. The level of miR-873-5p was determined using real time PCR. The expression of Gli1 was determined using western blot and immunohistochemistry. A specific siRNA targeting Gli1 was selected. The role of Gli1 and miR-873-5p on gastric cancer cell viability, apoptosis and cell cycle was determined using MTT assay and flow cytometry, respectively. The 3'untranslated region (3'UTR) of Gli1 was cloned into the pmirGLO plasmid. Dual luciferase reporter assay was applied to determine the target gene of miR-873-5p. The expression of miR-873-5p was decreased in gastric cancer, while the expression of Gli1 was significantly enhanced. Overexpression of miR-873-5P decreased cell viability, increased cell apoptosis and cell cycle arrest. Meanwhile, knockdown of Gli1 obviously induced SGC-7901 cell apoptosis and cell cycle arrest. Dual luciferase reporter assay showed that Gli1 was the target gene of miR-873-5p. More importantly, inhibition of miR-873-5p obviously decreased the protein expression of CyclinB1 and Bcl2 even in cells transfected with si-Gli1. To conclude, MiR-873-5p functions as a tumor suppressor in gastric cancer mainly by targeting Gli1.