〔Abstract〕 Objective To detect the expression of protein arginine methyltransferase 5(PRMT5) in gastric cancer tissues and gastric cancer cells, and to investigate the regulation of PRMT5 on the proliferation, migration, invasion and epithelial mesenchymal transition(EMT) of gastric cancer cells. Methods (1) The expression of PRMT5 in pathological tissues of chronic non-atrophic gastritis, and pregastric cancer, including chronic atrophic gastritis and intestinal metaplasia, and early gastric cancer was analyzed based on Bioinformatics Analysis by GEO database. Ualcan and HPA databases were employed to analyze the expression of PRMT5 in gastric cancer tissues. The expression of PRMT5 in gastric cancer cells was detected by Western blot.(2) The expression of PRMT5 in gastric cancer cells was regulated by plasmid, and its efficiency was verified by Western blot and RT-PCR. The protein expression of PRMT5 in gastric cancer cells was analyzedviaWestern blot. The abilities of migration and invasion were examined by scratch assay, Transwell and BD Matrigel invasion assays. Clone formation assay and CCK-8 assay were used to examine the proliferation of gastric cancer cells.(3) The expression of interstitial-related proteins and epithelial-related proteins was evaluatedviaWestern blot. Results GEO database found that PRMT5 expression increased gradually in chronic non-atrophic gastritis, precancerous lesions and early gastric cancer. Ualcan and HPA databases found that PRMT5 in gastric cancer tissues were higher than that in normal gastric tissues both at the mRNA and protein levels. PRMT5 upregulation elevated the migration, invasion and proliferation of gastric cancer cells, while PRMT5 downregulation inhibited those. In addition, PRMT5 upregulation raised the expression of interstitial-related proteins and decreased the expression of epithelial-related proteins while PRMT5 downregulation was the opposite. Conclusion PRMT5 is relatively highly expressed in gastric cancer tissues. Furthermore, PRMT5 can enhance the migration, invasion and proliferation ability of gastric cancer cells, and promote EMT in gastric cancer.