中文摘要：

目的 通过研究二甲双胍对子宫内膜癌（EC）孕激素耐药细胞增殖的影响以探讨二甲双胍能否改善EC细胞中孕激素的耐药。方法 在EC细胞系Ishikawa细胞的基础上,以醋酸甲羟孕酮（MPA）为诱导剂,采用逐步递增的方法持续给药,体外培养诱导建立EC孕激素耐药细胞;用CCK-8的方法研究细胞系Ishikawa细胞和MPA-R-Ishikawa细胞的生长增殖情况,以及MPA和二甲双胍对2种细胞增殖的影响。结果 1成功建立了EC孕激素耐药细胞（MPA-R-Ishikawa）,细胞系Ishikawa细胞和MPA-R-Ishikawa细胞的倍增时间差异无统计学意义（t=0.249,P=0.808）;2低浓度的MPA对耐药细胞MPA-RIshikawa的增殖有轻微的刺激作用,高浓度的MPA对耐药细胞MPA-R-Ishikawa的抑制作用不明显,而MPA对细胞系Ishikawa细胞具有显著的抑制作用;3二甲双胍对细胞系Ishikawa细胞和MPA-R-Ishikawa细胞的增殖均有抑制作用,具有浓度依赖性,但对后者的作用更显著。结论 二甲双胍能够抑制EC孕激素耐药细胞的增殖,可能会改善EC孕激素的耐药。

英文摘要：

Objective To explore the improvement effect of metformin on progestin-resistance of endometrial cancer cells by researc- hing the effect of metformin on proliferation of progestin-resistant cells of endometrial cancer. Methods Based on endometrial cancer Ish- ikawa cell line, MPA was used as revulsant to establish progestin-resistant cells of endometrial cancer in vitro by gradually increasing and continuous medication; CCK-8 assay was used to detect the proliferation of Ishikawa cells and MPA-R-Ishikawa ceils and the effects of MPA and metformin on proliferation of two kinds of cells. Results Progestin-resistant cells of endometrial cancer were successfully estab- lished, there was no statistically significant difference in the cell growth doubling time between Ishikawa cells and MPA-R-lshikawa cells （t = 0. 249, P = 0. 808 ） . Low concentration MPA stimulated proliferation of MPA-R-Ishikawa cells, the stimulation effect of high concentra- tion MPA on MPA-R-Ishikawa cells is insignificant, but MPA significantly inhibited Ishikawa cells ; metformin inhibited proliferation of Ish- ikawa cells and MPA-R-Ishikawa cells, showing a concentration-dependent manner, but the inhibiting effect on MPA-R-Ishikawa cells was more significant. Conclusion Metformin can inhibit the growth of progestin-resistant cells of endometrial cancer, which may improve progestin-resistance in endometrial cancer eases.