Objective: To observe the effect of exogenous gastrin-17 on the expression of E-Cadherin and N-Cadherin in human gastric cancer cell line SGC-7901, and discuss the related mechanisms. Methods: SGC-7901 cells were pre-treated with or without YM022 for 1 h and then incubated with G-17 for 30 min to detect the activation of JAK2/STAT3 signaling pathway, for 24 h to detect the expression of E-Cadherin and N-Cadherin, respectively by western blot analysis. SGC-7901 cells were transfected with CCK2R-siRNA or full-length cDNA of human CCK2R (pCMV6-CCK2R), followed by G-17 treatment to detect the expression of p-STAT3, E-Cadherin and N-Cadherin. Cells were pre-treated with AG490 for 1 h or knockdown of STAT3 with siRNA, then incubated with G-17 for 24 h to evaluate the expression of E-Cadherin and N-Cadherin. Results: Western blot assay showed the exogenous G-17 significantly decreased the expression of E-Cadherin and increased the expression of N-Cadherin, meanwhile, activated the JAK2/STAT3 signaling pathway. Specific antagonist or siRNA against CCK2R partly blocked gastrin-induced activation of STAT3 and the expression of E-Cadherin and N-Cadherin, which suggested the effect of gastrin was CCK2R dependent. Specific inhibitor of JAK2/STAT3 signaling pathway AG490 and siRNA against STAT3 partly attenuated the effect of gastrin on the expression of E-Cadherin and N-Cadherin. Conclusion: Gastrin acting on the cholecystokinin2 receptor, down-regulates expression of E-Cadherin and up-regulates the expression of N-Cadherin, via activation of JAK2/STAT3 signaling pathway induced EMT in human gastric cancer cells.