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作 者:王国增[1] 吴乾渝[1] 刘岚[1] 周奇[1] 李婷[1]
机构地区:[1]同济大学附属东方医院妇产科,上海200120
出 处:《同济大学学报(医学版)》2011年第4期43-47,共5页Journal of Tongji University(Medical Science)
摘 要:目的探讨二甲双胍在体外对人子宫内膜癌细胞增殖的影响及其可能的作用机制。方法二甲双胍干预人子宫内膜癌RL95-2和KLE细胞不同时间后,采用MTT法检测其对细胞增殖的影响,流式细胞术检测细胞周期,Western印迹法检测IGF-1Rβ、Akt和p-Akt的表达。结果二甲双胍显著抑制子宫内膜癌RL95-2和KLE细胞的增殖。流式细胞术检测显示二甲双胍使G_0/G_1期细胞比例升高,S期细胞比例降低。Western印迹法检测显示二甲双胍能够降低IGF-1Rβ和p-Akt的表达。结论二甲双胍能抑制子宫内膜癌细胞生长,其作用机制可能与下调IGF-1Rβ表达和抑制Akt活性有关。Objective To investigate the effect of metformin on proliferation of human endometrial carcinoma cell lines in vitro and explore the possible mechanisms. Methods Human endometrial carcinoma cell lines RL95-2 and KLE were used in the study. Cell proliferation was measured by MTT assay after exposure to metformin. Cell cycle was detected by flow cytometry. Expression levels of IGF-1Rβ, total Akt and phosphorylated Akt(p-Akt) were examined by Western blot. Results Metformin markedly inhibited cell proliferation in both cell lines. Flow cytometric analysis showed that mefformin increased the number of cells in G0/G1 and reduced the percentage of cells in S phase. Western blot demonstrated that metformin down-regulated the expression of IGF-1RI3 and p-Akt. Conclusion Mefformin can inhibit growth of human endometrial carcinoma cells, which might be associated with down-regulation of IGF-1Rβ and Akt activation.
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