miR-26b对HepG2细胞肿瘤干性的抑制作用  

The Inhibition of miR-26b on Tumor Stemness of HepG2 Cell

作　　者：嘉红云[1] 石永杰[1] 潘嘉韵 黄思聪[1] 

机构地区：[1]广州医科大学附属第二医院检验科,广东省广州市510260

出　　处：《医学理论与实践》2017年第11期1565-1567,共3页The Journal of Medical Theory and Practice

基　　金：广州市科技和信息化局项目(2014J4100063);广州医科大学青年科研项目(2015A05)资助

摘　　要：目的:探讨miR-26b对人肝癌细胞HepG2肿瘤干性的影响。方法:分别用miR-26b模拟物和抑制物瞬染HepG2细胞;体外成球实验检测HepG2细胞体外成球能力、real-time PCR检测肿瘤细胞干性基因Nanog/OCT4/BMI1/ABCG2的改变。结果:与对照组HepG2细胞对比,miR-26b过表达细胞的成球能力减弱,4种干性基因表达均下降;反之,miR-26b抑制细胞的成球能力明显增加,干性基因Nanog/OCT4/BMI1/ABCG2表达出现不同程度的上升。结论:miR-26b能降低HepG2肿瘤细胞的干性。Objective：To investigate the influence of miR-26b on HepG2 cell＇s sternness. Methods：Use mimics and inhibitors of miR-26b to transfer into HepG2. Sphere experiment and real-time PCR were used to detect sphere ability of HepG2 cells and the changing of stem gene Nanog/OCT4/BMI1/ABCG2. Results： Comparing with normal HepG2 cells, the sphere ability of miR-26b overexpression cells were decreasing sharply, the expression of stem gene Nanog/ OCT4/BMI1/ABCG2 were also reducing. On the contrary, the sphere ability of miR-26b inhibition cells were increasing and the expression of stem gene Nanog/OCT4/BMI1/ABCG2 were going up. Conclusion： miR-26b suppresses the tumor cell stemness of HepG2 cells.

关 键 词：HEPG2细胞 miR-26b 肿瘤干性 

分 类 号：R73-37[医药卫生—肿瘤]