Objective:To observe the effect of the artesunate(ART) on cellular proliferation in vitro,to search for the possible anti-tumor mechanism of ART on endometrial carcinoma at the molecular level and to provide the experimental and theoretical foundations for the clinical applications of ART.Methods:The cell proliferation was observed by microscope;MTT was used to examine the effects of ART on proliferation of HEC-1B cells,and flow cytometric analysis was used to detect cell cycle and apoptosis.The human endometrial carcinoma HEC-1B cells were conventionally cultured;ART was administered with a concentration of 40 μg/ml before the total RNA were extracted.mRNA expression of Survivin,Caspase-3,N-Cadherin,E-Cadherin,Fibronectin1 and Cox-2 were detected using RT-PCR.Results:ART reduced proliferation in human endometrial carcinoma cell line HEC-1B in a dose-and time-dependent effect.The cells of G0/G1 stage were significantly increased(P<0.05),but the cells of G2/M stages were significantly decreased(P<0.05),so it has shown that the cell cycle was probably blocked in G0/G1 stage.After intervention with ART at 20 and 80 μg/ml for 48 h,cellular apoptosis rate respectively was(36.42±0.77)% and(11.77±0.58)%,and the difference was statistically significant compared with the control([6.64±0.19]%,P<0.01).The expression of Cox-2 mRNA in the ART group was lower than those of control group,yet the expression of Caspase-3 and E-Cadherin mRNA in the ART group was higher than those of control group.Conclusion:ART can inhibit HEC-1B cell growth and proliferation in a dose-and time-dependent manner.Furthermore,ART can induce apoptosis in a dose-dependent manner.ART is able to downregulate Cox-2 mRNA expression and to upregulate E-Cadherin and Caspase-3 mRNA expression.So we can conclude that ART could induce the endometrial carcinoma HEC-1B cell apoptosis and inhibit tumor cell proliferation. Objective: To observe the effect of the artesunate (ART) on cellular proliferation in vitro, to search for the possible anti-tumor mechanism of ART on endometrial carcinoma at the molecular level and to provide the experimental and theoretical foundations for the clinical applications of ART . Methods: The cell proliferation was observed by microscope; MTT was used to examine the effects of ART on proliferation of HEC-1B cells, and flow cytometric analysis was used to detect cell cycle and apoptosis. The human endometrial carcinoma HEC-1B cells were conventionally cultured; ART was administered with a concentration of 40 μg / ml before the total RNA were extracted. mRNA expression of Survivin, Caspase-3, N-Cadherin, E-Cadherin, Fibronectin1 and Cox-2 were detected using RT-PCR. Results: ART reduced proliferation in human endometrial carcinoma cell line HEC-1B in a dose-and time-dependent effect. The cells of G0 / G1 stages were significantly increased (P <0.05), but the cells of G2 / M stages were significantlydecreased (P <0.05), so it has shown that the cell cycle was probably blocked in G0 / G1 stage. After intervention with ART at 20 and 80 μg / ml for 48 h, cellular apoptosis rates were respectively (36.42 ± 0.77)% (11.77 ± 0.58)%, and the difference was statistically significant compared with the control ([6.64 ± 0.19]%, P <0.01). The expression of Cox-2 mRNA in the ART group was lower than those of control group, yet the expression of Caspase-3 and E-Cadherin mRNA in the ART group was higher than those of control group. Conlusion: ART can inhibit HEC-1B cell growth and proliferation in a dose-and time-dependent manner. induce apoptosis in a dose-dependent manner. AR is able to downregulate Cox-2 mRNA expression and upregulate E-Cadherin and Caspase-3 mRNA expression. So we can conclude that ART could induce the endometrial carcinoma HEC-1B cell apoptosis and inhibit tumor cell proliferation.