miR-545-3p抑制食管癌细胞Eca109和TE-1生长的机制研究  

Mechanism of miR-545-3p in inhibiting growth of esophageal cancer cells Eca109 and TE-1

作　　者：王向辉[1] 黄江平[1] 崔丰和[1] 钱海云[1] 

机构地区：[1]华中科技大学同济医学院附属荆州医院心胸大血管外科,434020

出　　处：《国际消化病杂志》2017年第5期316-320,共5页International Journal of Digestive Diseases

摘　　要：目的探讨miR-545-3p抑制食管癌细胞Eca109和TE-1生长的机制。方法以食管癌细胞Eca109和TE-1作为研究对象,转染miR-NC(对照组)或miR-545-3p(实验组);荧光实时定量聚合酶链反应(qRT-PCR)和蛋白质印迹法(Western blotting)检测细胞周期蛋白依赖激酶4(CDK4)、细胞周期素D1(Cyclin D1)和p21活化蛋白激酶2(PAK2)mRNA及蛋白表达水平;流式细胞术检测细胞周期和细胞凋亡变化;细胞增殖实验(MTS法)和集落形成实验检测细胞增殖能力。结果过表达miR-545-3p后,CDK4、Cyclin D1和PAK2 mRNA及蛋白的表达明显下调(P<0.05),促进细胞周期的进展和细胞凋亡的增加(P<0.05),明显抑制食管癌细胞的增殖能力(P<0.05)。结论miR-545-3p通过靶向干扰CDK4、Cyclin D1和PAK2的表达来抑制食管癌细胞的生长,是食管癌基因治疗的潜在靶点。Objective This paper intents to investigate the mechanism of miR-545-3 p in inhibiting the growth of esophageal cancer cells Eca109 and TE-1.Methods miR-NC（control group）or miR-545-3 p（experimental group）was transfected into esophageal cancer cells Eca109 and TE-1.The real-time quantitative polymerase chain reaction（qRT-PCR）and western blotting were used to detect the expression of cyclin-dependent kinase 4（CDK4）,cyclin D1 and p21 protein kinase 2（PAK2）mRNA,and protein.The cell cycle and apoptosis were detected by using flow cytometry.The MTS and colony formation assay were used to detect the cell proliferation ability.Results The overexpression of miR-545-3 p significantly reduced the expression of CDK4,cyclin D1 and PAK2 mRNA,and protein（P〈0.05）,promoted the progress of cell cycle and the increase of apoptosis（P〈0.05）,and suppressed the proliferation ability of esophageal cancer cells（P〈0.05）.Conclusion miR-545-3 p inhibits the growth of esophageal cancer cells by interfering the espression of CDK4,Cyclin D1,and PAK2,which is a potential target for gene therapy of esophageal cancer.

关 键 词：微RNA CDK4 CYCLIN D1 PAK2 食管癌 

分 类 号：R735.1[医药卫生—肿瘤]