Abstract: Objective：To explore the mechanism of bisphenol A on the proliferation in human endometrial cancer cells (Ishikawa and RL952) via PI3K/AKT signaling pathway. Methods：CCK8 assay was used to detect the proliferation in Ishikawa and RL952 cells, and Western blotting was applied to observe the expression of phosphorylation-AKT. Results：Ishikawa and RL952 cells proliferation increased significantly with treatment of 1 μmol/L BPA after 48 h, and cell proliferation was (0.758±0.023) and (0.692±0.042) respectively (P＜0.01). The proliferation effect decreased when BPA was more than 1 μmol/L. Ishikawa and RL952 cells did not increase after treated for 24 h. Cytotoxic effects were showed after BPA treated for 72 h. After 1 μmol/L BPA treated for 48 h, p-AKT expression was increased significantly compared with controls（P＜0.05）. When PI3K was blocked by LY294002, p-AKT expression was decreased, but it is not significant compared to controls (P＞0.05). Conclusions：Bisphenol A induced endometrial cancer cell proliferation by activating PI3K/AKT pathway.

Key words: Endometrial neoplasms, Phosphatidylinositol 3-kinase, Cell proliferation, Bisphenol A