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作 者:冉志华[1] 刘炯[1] 冯缨[1] 李晓波[1] 邹健[1] 萧树东[1]
机构地区:[1]上海第二医科大学仁济医院上海市消化疾病研究所,200001
出 处:《中华消化杂志》2002年第9期539-542,共4页Chinese Journal of Digestion
基 金:国家教委青年骨干教师项目资助
摘 要:目的 探讨具有选择性杀伤和抑制肿瘤细胞生长特性的细小病毒H 1所诱导的胃癌细胞死亡的信号传导通路及可能机制。方法 采用RT PCR的方法 ,检测H 1病毒感染后胃癌细胞HGC2 7的有丝分裂原激活蛋白激酶 (MAPK)信号传导途径相关基因在mRNA水平的表达改变。结果 MAPK信号传导相关基因的扩增结果显示 :在H 1病毒感染HGC2 7细胞 48h后 ,细胞CREB基因的表达明显增高 ,ERK1、STAT2、p38 γ、MEK2、β RAF、MTK1基因的表达明显降低 ,而JNK2、ETS、ERK2基因在mRNA水平的表达无明显改变。结论 细小病毒H 1的细胞毒作用可能与其影响胃癌细胞MAPK信号传导途径中相关基因的表达有关。即H 1病毒通过干预癌细胞信号传导的特定通路而诱导细胞死亡。由此我们认为 ,可修饰改造的细小病毒H 1。Objective To explore the antineoplastic parvovirus H-1 induced cell death signaling pathways and their possible mechanisms in gastric carcinoma cells. Methods By using RT-PCR method, the mRNA expressional changes of mitogen-activated protein kinase (MAPK) signaling transduction pathway related genes were measured in gastric adenocarcinoma HGC27 cells infected by H-1 virus. Results The RT-PCR amplification results displayed that 48 h after HGC-27 cells were infected by H-1 virus, the expression of CREB was increased, the expression of ERK1, STAT2, p38-γ, MEK2, β-RAF and MTK1 were remarkably decreased, however, the expression of JNK2, ETS and ERK2 had no apparently change. Conclusions The cytotoxic effects of parvovirus H-1 might affect the gene expression involved in MAPK signal transduction pathway in gastric carcinoma HGC27 cells. It indicates that H-1 virus might interfere with specific cellular signal transduction pathways of gastric carcinoma cell to induce cell death. In conclusion, it was considered that modified and reconstructed parvovirus H-1 would be a very valuable tool in the anti-tumor study.
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