AAV介导的BATF2/SARI过表达抑制肝癌细胞HepG2增殖  

Overexpression of AAV- BATF2/SARI inhibits HepG2 cell proliferation

作　　者：龚嘉玲[1] 白雪佳[1] 路钊[1] 张晨光[2] 丁卫[2] 牛静[1] 

机构地区：[1]首都医科大学基础医学院生物化学与分子生物学系,北京100069 [2]首都医科大学基础医学院遗传学系,北京100069

出　　处：《北京医学》2013年第6期431-433,I0001,共4页Beijing Medical Journal

基　　金：国家自然科学基金(No.31201032;No.81201816;No.30970161)

摘　　要：目的探讨腺相关病毒(adeno-associated virus,AAV)介导的BATF2/SARI过表达对肝癌细胞HepG2细胞活力的影响及其分子机制。方法通过分子克隆技术构建AAV介导的BATF2/SARI过表达载体,用包装纯化后的AAV-BATF2感染HepG2细胞,MTT检测其对细胞活力的作用,荧光素酶分析其对NFκB转录活性的影响。结果重组AAV-BATF2载体构建成功,AAV-BATF2感染的HepG2细胞生长活力受到明显抑制,NFκB转录活性明显下调。结论重组AAV-BATF2病毒感染人肝癌细胞HepG2可抑制肿瘤细胞增殖,其对NFκB转录活性的抑制可能是其发挥作用的机制之一。Objective To investigate the effect of AAV- BATF2/SARI on cell viability in HepG2 cells and the mechanisms of this effect. Methods The AAV- BATF2/SARI vector was constructed by molecular techniques and the recombinant infectious AAV particles was produced. The cell viability was examined by MTT assays and luciferase reporter activity driven by NFKB interactive sequences was examed by luciferase assays. Results The infection of AAV-BATF2 in HepG2 cells significantly reduced the cell viability. Meanwhile, the luciferase reporter activity driven by NFKB was dramatically decreased. Conclusion Recombinant AAV-BATF2 infected HepG2 cells inhibit tumor cell proliferation, and its inhibition on NFKB transcriptional activity may be one of the mechanisms.

关 键 词：腺相关病毒 BATF2 SARI 肝癌细胞 细胞活力 

分 类 号：R735.7[医药卫生—肿瘤]