miR-375在子宫内膜癌HEC-1-B细胞中的生物学功能

The biological function of miR-375 in endometrial carcinoma HEC-1-B cells

目的:探讨miR-375在Ⅱ型子宫内膜癌中的表达及对HEC-1-B细胞增殖、凋亡的影响。方法:miRNA芯片分析Ⅱ型子宫内膜癌miRNA表达谱。利用lipofectamine 2000转染HEC-1-B细胞。实时荧光定量PCR检测转染后miR-375的表达。CCK-8检测转染后细胞增殖能力的改变。流式细胞仪检测细胞转染效率及转染后细胞凋亡情况。结果:miR-375在Ⅱ型子宫内膜癌组织中低表达。转染效率达73.43%。转染后实验组miR-375表达量较NC组和对照组明显增加(P<0.05)。实验组较NC组生长明显受抑(P<0.05)。实验组较NC组、对照组凋亡明显增加(P<0.05)。结论:初步证明miR-375抑制Ⅱ型子宫内膜癌细胞增殖并促进凋亡,可能成为Ⅱ型子宫内膜癌基因治疗的靶点。

Objective To explore the expression of miR-375 in type II endometrial carcinoma and its effects on the proliferation and apoptosis of HEC-1-B cells. Methods miRNA expression of type II endometrial carcinoma was analyzed by miRNA microarray, miR-375 mimics was transfected into HEC-1-B cells by lipofectamine 2000, then the expression of miR-375 was detected by quantitative real-time PCR. The proliferation was detected by CCK-8, and the apoptosis and transfection efficiency were detected by flow cytometry. Results MiR-375 was down- regulated in type II endometrial carcinoma, and the transfection efficiency was 73.43%. The expression of miR-375 in experiment group after transfection was increased than those in NC group and control group （P〈 0.05）. As compared to that in NC group, the inhibitory effect of miR-375 in experiment group was confirmed by CCK-8 （P 〈 0.05）. There was significant difference in the apoptosis rate （P 〈 0.05） between experiment group and NC group, control group. Conclusion MiR-375 might inhibit the proliferation and promote the apoptosis of type II endometrial carcinoma cells, which may be the new target of gene therapy for type II endometrial carcinoma.