目的:研究抵抗素对子宫内膜癌细胞增殖的影响及其对子宫内膜癌细胞PI3K/Akt信号传导通路的作用。方法:CCK-8法检测不同浓度抵抗素(0ng/ml、10ng/ml、50ng/ml、100ng/ml、200ng/ml)对Ishikawa和KLE两种子宫内膜癌细胞系增殖的影响。Western blot法检测不同浓度抵抗素作用下PI3K/Akt信号通路的变化及PI3K/Akt信号通路抑制剂对抵抗素活化PI3K/Akt信号通路作用的影响。结果:抵抗素能促进两种子宫内膜癌细胞系Ishikawa和KLE的生长,并呈时间和浓度依赖性。抵抗素可促进两种子宫内膜癌细胞系中PI3K/Akt信号通路的激活。PI3K/Akt信号通路抑制剂LY29004可减弱抵抗素诱导的Akt磷酸化水平。结论:抵抗素能促进子宫内膜癌细胞增殖,这种作用可通过激活PI3K/Akt信号通路来实现。 Objective: To study the effect of resistin on the proliferation of endometrial carcinoma cells and its effect on PI3K / Akt signaling pathway in endometrial carcinoma cells. Methods: The effects of different concentrations of resistin (0 ng / ml, 10 ng / ml, 50 ng / ml, 100 ng / ml, 200 ng / ml) on the proliferation of Ishikawa and KLE endometrial carcinoma cell lines were determined by CCK- The changes of PI3K / Akt signaling pathway by different concentrations of resistin and the effect of PI3K / Akt signaling pathway inhibitors on the activation of PI3K / Akt signaling pathway by Western blotting. RESULTS: Resistin promoted the growth of both endometrial cancer cell lines Ishikawa and KLE in a time and concentration dependent manner. Resistin promotes the activation of the PI3K / Akt signaling pathway in two endometrial cancer cell lines. PI3K / Akt signaling pathway inhibitor LY29004 attenuated resistin-induced Akt phosphorylation. Conclusion: Resistin can promote the proliferation of endometrial cancer cells, and this effect can be achieved by activating the PI3K / Akt signaling pathway.