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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 and molecular mechanism of BATF2 / SARI-mediated over-expression of adeno-associated virus (AAV) on HepG2 cell viability. Methods AAV-mediated over-expression vector BATF2 / SARI was constructed by molecular cloning technique. HepG2 cells were infected with packaged purified AAV-BATF2. MTT assay was used to determine the effect on cell viability. The effect of luciferase on NFκB transcription was analyzed. Results The recombinant AAV-BATF2 vector was successfully constructed. The viability of HepG2 cells infected with AAV-BATF2 was significantly inhibited and the NFκB transcription activity was significantly down-regulated. Conclusion Recombinant AAV-BATF2 can infect human hepatoma HepG2 cells to inhibit the proliferation of tumor cells. Inhibition of NFκB transcriptional activity may be one of the mechanisms by which AAV-BATF2 may play a role.