Objective To explore the mechanism by which miR-16 regulates the expression of Bcl-2 on the biological behavior of gastric cancer cells. Methods qPCR was used to detect the transfection efficiency of miR-16 in gastric cancer SGC7901 cells. CCK8 was used to detect the activity of SGC7901. Scratch assay was used to detect the effect of miR-16 on migration of SGC7901 cells. The effect of miR-16 on the apoptosis of SGC7901 cells was detected by flow cytometry. The effect of miR-16 on Bcl-2 protein expression was detected by Western blotting. Apoptosis mrelated proteins were detected by Western blotting.Results After miR-16 overexpressing in gastric cancer SGC7901 cells by miR-16 mimic, the cell viability and migration ability significantly decreased, while the apoptosis rate increased significantly. Cotransfection of Bcl-2 siRNA and miR-16 inhibitor changed the effect of miR-16 on the migration ability, cell viability and apoptosis of SGC7901 cells.Conclusion miR-16 can induce gastric cancer SGC7901 cell apoptosi, inhibit cell viability and migration ability by regulating the expression of Bcl-2.