5-Aza-CdR抑制HepG2细胞DLK1基因表达及细胞生长  

5-Aza-CdR inhibits DLK1 expression and cell growth of human hepatocarcinoma cell line HepG2

作　　者：黄铀新[1] 罗耀玲[2] 刘瑶[3] 

机构地区：[1]赣南医学院第一附属医院核医学科,江西赣州341000 [2]赣南医学院第一附属医院临床医学研究中心,江西赣州341000 [3]赣南医学院第一附属医院消化内科,江西赣州341000

出　　处：《基础医学与临床》2013年第8期966-970,共5页Basic and Clinical Medicine

基　　金：国家自然科学基金(81000908)

摘　　要：目的探讨去甲基化药物5-氮杂-2'-脱氧胞苷(5-Aza-CdR)对DLK1基因及肝癌细胞系HepG2增殖、侵袭的影响。方法不同浓度的5-Aza-CdR及PBS作用HepG2细胞后,RT-PCR、Western blot检测DLK1基因及蛋白的表达水平;MTT、Transwell和流式细胞术检测HepG2细胞的生长、侵袭力及细胞周期的变化。结果 HepG2细胞经5-Aza-CdR处理后,DLK1 mRNA、蛋白表达量降低;MTT试验显示细胞生长速度依5-Aza-CdR浓度出现不同程度减慢;流式结果表明G1期细胞减少,S期细胞增加,出现S期阻滞;Transwell证实侵袭能力显著降低(P<0.05)。结论去甲基化药物5-Aza-CdR能有效地抑制DLK1基因的表达,从而抑制肿瘤细胞HepG2生长、增殖、侵袭能力。Objective To investigate if demethylation drug 5-Aza-2＇-deoxycytidine （5-Aza-CdR） may inhibit the expression of DLK1 and cell proliferation,invasion of hepatoma cell line HepG2. Methods After different concen- trations of 5-Aza-CdR were applied to treat HepG2 cells, RT-PCR, Western blot were used for the detection of DLK1 mRNA and protein level change ; MTT, Transwell and flow cytometry were used for detection of cell growth, cycle and invasiveness. Results After treatment with 5 μmol/L 5-Aza-CdR, the expression of DLK1 mRNA and protein decreased, the cell growth rate was slowed, the number of G1 phase cells decreased where the S phase cells increased, Transwell confirmed invasive ability decreased significantly （ P 〈 0. 05 ）. Conclusions 5-Aza-CdR can effectively inhibit DLK1 gene expression, thereby inhibiting tumor cell growth, proliferation, invasion of HepG2.

关 键 词：HEPG2细胞 5-AZA-CDR DLK1基因 

分 类 号：R735.7[医药卫生—肿瘤]