miR-34c对Ⅱ型子宫内膜癌HEC-1-B细胞生长和凋亡的影响  

The influence of miR-34c on growth and apoptosis of type Ⅱ endometrial carcinoma cell line HEC-1-B

作　　者：李甫钥[1] 薛纪森[1] 黄亦波[1] 陈慧君[1] 郑飞云[1] 

机构地区：[1]温州医科大学附属第一医院妇科,浙江温州325015

出　　处：《温州医学院学报》2014年第2期86-90,共5页Journal of Wenzhou Medical College

基　　金：浙江省自然科学基金资助项目(Y2090699)

摘　　要：目的:研究miR-34c对Ⅱ型子宫内膜癌HEC-1-B细胞的生长及凋亡的影响。方法:用hsa-miR-34c mimics转染HEC-1-B细胞。流式细胞技术测定细胞转染率,实时荧光定量PCR验证转染后miR-34c的表达。CCK-8检测细胞增殖能力的改变。细胞克隆形成实验观察miR-34c对细胞生长的长期抑制。流式细胞技术测细胞凋亡。结果:细胞转染率为81.16%。相对于对照组,转染后实验组miR-34c表达明显增加,细胞增殖、克隆形成能力减弱,凋亡增加(P<0.05)。结论:miR-34c能明显抑制Ⅱ型子宫内膜癌细胞的增殖,促进细胞凋亡,是Ⅱ型子宫内膜癌的潜在抑癌基因。Objective： To investigate the effect miR-34c on the growth and apoptosis of type Ⅱ endome-trial carcinoma cells （HEC-1-B cell line）. Methods： Up-regulated the expression of miR-34c by transfecting cells with hsa-miR-34c mimics, the transfection efficiency was detected by flow cytometry and further verified by quantitative real-time PCR （qRT-PCR）. Cell proliferation assay by CCK-8 and colony formation assay applied to demonstrate that miR-34c could inhibit the growth of HEC-1-B cells. Cells apoptosis assay was analyzed by flow cytometry. Results： The transfection efficiency was 81.16%. The overexpression of miR- 34c （detected by qRT-PCR） could inhibit cell proliferation, colony formation and promote cells apoptosis （P 〈0.05）. Conclusion： MiR-34c can inhibit the growth and promote apoptosis of HEC-1-B cells significantly, and function is a potential tumor suppressor in type Ⅱ endometrial carcinoma.

关 键 词：miR-34c Ⅱ型子宫内膜肿瘤 细胞 增殖 凋亡 

分 类 号：R711[医药卫生—妇产科学]