Objective: To explore the promotion role of PGE2 stimulating on the growth of endometrial cancer cells in vitro and its molecular mechanisms. Methods: Detection the expression of β-catenin protein between normal endometrium and endometrial cancer by immunochemical EnVision method. Cell growth rates were assessed by WST-8 method. The expression levels of β-catenin,p-β-catenin,GSK-3β and p-GSK-3β were examined by Western Blot analysis. Immunofluorescence technique was applied to compare the location of β-catenin protein between the control group and the PGE2 treated group. Results: β-catenin only expressed on the membrane of endometrial tissue,while expressed strongly in the cytoplasm and nuclear of endometrial cancer tissues. When cells were treated with DMSO,PGE2,Butaprost and AH6809 for 24 h,the cell growth rates were 100% ,183.9%,151.9% and 72.1%,respectively. With the stimulation of PGE2,β-catenin increased to 235.7%,p-β-catenin to 76.8%,and p-GSK-3β to 204.3%,and the datum were 279.7%,33.6%,236.7% in Butaprost combined PGE2 treatment group,and 185.2%,73.9%,116.2% in AH6809 combined PGE2 treatment group. β-catenin protein had much stronger signals in PGE2 treated group than control group,with the signals located in cytoplasm and nuclei by immunofluorescence observation. Conclusion: PGE2 could prmote proliferation of Ishikawa cells accompanied with β-catenin overexpressing and transfering into nuclear,and both Wnt/β-catenin signaling pathway and EP2 receptor activating might be involved in the process.