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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。
Objective To investigate the effect of metformin on the proliferation of progestin-resistant cells in endometrial carcinoma (EC) to explore whether metformin can improve the resistance of progesterone in EC cells. Methods ECS cell line Ishikawa cells were treated with medroxyprogesterone acetate (MPA) as an inducer, and then the drug was administered continuously. The EC progestin-resistant cells were induced in vitro by CCK-8 The growth and proliferation of Ishikawa cells and MPA-R-Ishikawa cells were studied, and the effects of MPA and metformin on the proliferation of 2 kinds of cells were studied. Results1 The doubling time of EC progestin resistant cells (MPA-R-Ishikawa), Ishikawa cells and MPA-R-Ishikawa cells was not significantly different (t = 0.249, P = 0.808) The concentration of MPA had a slight stimulation on the proliferation of MPA-RIshikawa cells. The MPA-R-Ishikawa inhibited the proliferation of MPA-R-Ishikawa cells with high concentration of MPA, whereas MPA had a significant inhibitory effect on the cell line Ishikawa cells. 3 Metformin inhibited the proliferation of Ishikawa cells and MPA-R-Ishikawa cells in a concentration-dependent manner, but the effect was more pronounced on the latter. Conclusion Metformin can inhibit the proliferation of EC progestin-resistant cells and may improve the EC progestin resistance.