Background and objective: Endometrial carcinoma is the most common gynecologic malignancy in the world. Although the insulinresistant state or hyperinsulinemia was recently suggested as a potent risk factor for endometrial carcinogenesis and progression, there is only limited supporting evidence and the mechanism is unclear. In this study, we explored the roles of phosphatidylinositol 3-kinase （PI3K）/Akt signaling pathway in the response of a human endometrial cancer cell line, Ishikawa 3-H-12 cells, to insulin. Conclusion: Insulin activates PI3K/Akt signaling pathway and is a mitogenic and anti-apoptotic agent for Ishikawa 3-H-12 endometrial cancer cells.