Abstract : Objective To investigate the expression level of microRNA-1184 ( miR-1184) in gastric cancer cells and its role in the proliferation, migration, cell cycle and apoptosis of gastric cancer cells. Methods The expression levels of miR-1184 in gastric cancer tissues and GES-1 human gastric mucosal epithelial cells were detected by real-time fluorescent quantitative PCR ( qRT-PCR). The proliferation and migration abilities of gastric cancer cells were determined by the CCK-8 assay, plate colony formation assay , Transwell migration assay, and cell scratch test. The changes in the cell cycle and apoptosis rate of gastric cancer cells were detected by flow cytometry. The expression levels of epithelial-mesenchymal transition ( EMT), cell cycle and apoptosis-related proteins were determined by Westem blot. The targeting relationship between miR-11 84 and isocit rate dehydrogenase 3 ( NAD+) alpha ( IDH3A) gene was detected by the double luciferase reporter gene assay. Results The expression levels of miR-1184 in gastric cancer tssues (t=2.54, P<0.05) and gastric cancer BGC-823 and MGC-803 cells (t= 13.99, P<0.001; t=14.85, P<0.01 ) were significantly lower than those in the adjacent tissues of gastric cancer and GES-1 cells. Compared with the control group, the transfection of miR-1 184 inhibitor promoted the proliferation (t=9.28, P<0.05), migration (t=9.24, P<0.001), EMT process, and G,/S phase transition of the cell cycle of gastric cancer cells and reduced cell apoptosis (t=6.57, P<0.01). The transfection of miR-1184 mimics inhibited the proliferation (t= 7.34, P<0.001), migration (t= 9.24, P<0.001), EMT process, and G,/S phase transition of the cell cycle of gastrice cancer cells and increased cell apoptosis (t= 20.33, P<0.000 1). miR-1184 could targetedly bind to IDH3A. The miR-1184 inhibitor could signifcantly increase the expression level of IDH3A protein in gastric cancer cells ( t= 11.32, P<0.001), while the miR-11 84 mimics reduced it (t=20.91, P<0.000 1). Conclusion miR-1184 is low expressed in gastric cancer tssues and cells，which can afect the biological behaviors of gastric cancer cells such a proliferation, migration, EMT proces, G;/S phase transition of the cell cycle, and apoptosis.