细小病毒H‐1感染对胃癌细胞MAPK信号通路相关基因表达的影响

Z. Ran, Jiong Liu, Ying Feng, Jian Zou, S. Xiao
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引用次数: 1

摘要

目的:探讨抗肿瘤细小病毒H-1对胃癌细胞的细胞毒性作用。方法:采用MTT法和FACS法检测H-1病毒对胃癌细胞株HGC27的细胞毒性。采用RT-PCR方法检测了H-1病毒感染HGC27细胞中丝裂原活化蛋白激酶(MAPK)信号转导通路相关基因的mRNA表达。结果:HGC27细胞对H-1病毒的细胞毒性敏感,但细胞周期分布无明显变化。RT-PCR结果显示,h -1病毒感染HGC27细胞48 h后,creb的表达升高,erk1、stat2、p38-γ、mek2、B-raf和mtk1的表达显著降低。而jnk2、ets和erk2的表达均未发生变化。结论:细小病毒H-1对HGC27细胞的细胞毒作用机制可能是通过干扰特定的细胞信号转导途径导致细胞死亡。修饰重组的细小病毒H-1可作为抗肿瘤生化治疗的重要工具。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Impact of parvovirus H‐1 infection on the expression of genes related to the MAPK signaling pathway in gastric cancer cells
OBJECTIVE:  To investigate the cell cytotoxicity induced by the antineoplastic parvovirus H-1 in gastric carcinoma cells. METHODS:  The cytotoxicity of the H-1 virus in the gastric cancer cell strain HGC27 was measured by MTT test and FACS analysis. The mRNA expressions of genes related to the mitogen-activated protein kinase (MAPK) signaling transduction pathway were measured by RT-PCR in HGC27 cells infected by the H-1 virus. RESULTS:  HGC27 cells were sensitive to the cytotoxicity of the H-1 virus, although the cell cycle distribution was not significantly changed. The RT-PCR results showed that 48 h after H-1 virus infection of HGC27 cells the expression of creb was increased and that of erk1, stat2, p38-γ, mek2, B-raf and mtk1 was remarkably decreased. However, the expression of each of jnk2, ets and erk2 was unchanged. CONCLUSIONS:  The mechanism of the cytotoxic effect of parvovirus H-1 in HGC27 cells might be interference with specific cellular signaling trans­duction pathways, which would induce cell death. A modified and reconstructed parvovirus H-1 could be a very useful tool for antitumor biochemical therapy.
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