重组慢病毒LV-hTERT-tumstatin的构建及其对人肝癌HepG2细胞增殖和凋亡的影响  

Effect of LV-hTERT-tumstatin mediated by lentivirus on proliferation and apoptosis of hepatocarcinoma HepG2 cells

作　　者：孟昱希 邓志华[1] 牛鑫[1] 

机构地区：[1]山西医科大学,山西太原030001

出　　处：《中国现代医药杂志》2014年第5期7-9,共3页Modern Medicine Journal of China

基　　金：山西省自然科学基金资助项目(编号:2012011038-6)

摘　　要：目的构建重组慢病毒LV-hTERT-tumstatin并探讨其对人肝癌HepG2细胞增殖和凋亡的影响。方法用不同病毒感染复数(MOI)LV-hTERT-tumstatin感染肝癌细胞HepG2及正常肝细胞L02,荧光显微镜下观察转染情况,MTT法检测两种细胞增殖情况,流式细胞术检测两种细胞凋亡情况。结果重组慢病毒LV-hTERT-tumstatin转染后在肝癌HepG2细胞中特异表达,在L02细胞中无表达。肝癌细胞HepG2的生长抑制率随MOI增加而逐渐增加,L02细胞生长无明显变化。慢病毒治疗组HepG2细胞凋亡率达(48.39±3.32)%,明显高于空白对照组(3.96±0.94)%(P<0.05),而对L02细胞作用不明显(P>0.05)。结论重组慢病毒LV-hTERT-tumstatin可靶向抑制肝癌HepG2细胞增殖和促进HepG2细胞凋亡。Objective To construct a recombinant lentivirus LV-hTERT-tumstatin and explore its effect on proliferation and apoptosis of HepG2 cells. Methods Used different MOI recombinant lentivirus infected HepG2 cells and L02 cells and detected the infection by fluorescence microscope. The proliferation and apoptosis of both HepG2 cells and L02 cells were detected by MTT and flow cytometry respectively. Results Recombinant lentivirus LV-hTERT-tumstatin was specifically expressed in HepG2 cells,while almost no expression in L02 cells. The proliferation inhibitory rate of HepG2 cells was increased along with the increase of the MOI,while no change on L02 cells. The apoptosis rate of treatment group was（48.39±3.32）%, significantly higher than that of the control group（3.96±0.94）%（P〈0.05）,but almost no change in normal hepatocyte（P〈0.05）. Conclusion LV-hTERT-tumstatin can selectively inhibit the proliferation and induce the apoptosis of human HepG2 cells.

关 键 词：肿瘤抑素 癌 肝细胞 增殖 凋亡 

分 类 号：R735.7[医药卫生—肿瘤]