miR-34c对人喉癌细胞株Hep-2细胞的影响  

Impact of miR-34con proliferation of laryngeal carcinoma cell line Hep-2

作　　者：王友娟 吴秋华 杨娟 罗松 

机构地区：[1]扬州东方医院肿瘤内科,江苏省225000 [2]淮阴医院耳鼻喉科

出　　处：《江苏医药》2014年第4期392-394,共3页Jiangsu Medical Journal

摘　　要：目的研究miR-34c对喉癌细胞株人喉癌表皮细胞(Hep-2)的细胞周期及细胞增殖的影响。方法将Hep-2分为转染miR-34c寡聚核苷酸组(A组)、转染无义序列组(B组)和空白对照组(C组)。采用RT-PCR、MTT法、流式细胞术及Western blot技术评价各组细胞增殖和细胞周期的生物学变化。结果转染miR-34c寡聚核苷酸后,Hep-2中miR-34c的表达上调;与C组相比,A组细胞增殖水平明显抑制。miR-34c寡聚核苷酸能够有效诱导Hep-2细胞周期阻滞在G1/G0期;A组细胞分裂周期蛋白42(CDC42)表达水平下调,cyclin依赖型激酶(CDK4)表达水平降低。结论 miR-34c寡聚核苷酸能够抑制喉癌细胞Hep-2的增殖;miR-34c是潜在的人喉癌细胞基因治疗的候选靶点。Objective To investigate the impact of miR-34c on the proliferation of laryngeal carcinoma cell line Hep-2. Methods The laryngeal carcinoma cell line Hely2 was assigned into three groups of A（transfected Hep-2 with oligonucleotide of miR-34c）, B（transfeeted Hep-2 with nonsense sequence） and C（blank control）. The expression of miR-34c was identified by RT-PCR and relevant protein expression was evaluated by Western blot. The cell proliferation and cell cycle were determined by MTT assay and flow cytometry, respectively. Results The miR-34c was obviously elevated atter transfection of rniR-34c mimics. The proliferation was significantly lower in group A than that in group C. Compared to groups of B and C, the miR-34c mimics in group A could effectively induce the cell cycle to arrest at G0/G1 phase. The protein expression of CDCA2 and regulatory molecules for cell cycle progression including CDK4 were decreased at same time. Conclusions MiR-34c inhibits the proliferation activity of Hep-2 cell, suggesting that miR-34c can be taken as a potential candidate for gene therapy of laryngeal carcinoma.

关 键 词：MiR-34c 喉癌 

分 类 号：R767[医药卫生—耳鼻咽喉科]