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作 者:汪砥[1] 刘蓓[1] 李跃辉[1] 周国华[1] 谢平丽[1] 李官成[1] 胡锦跃[1]
出 处:《医学临床研究》2007年第10期1677-1679,共3页Journal of Clinical Research
摘 要:【目的】利用基因转染技术将人源趋化因子受体CXCR4基因转染小鼠黑色素瘤细胞B16,研究异源CXCR4基因转染对肿瘤致瘤性的影响。【方法】脂质体转染法将人CXCR4基因导入小鼠黑色素瘤B16细胞中,RT-PCR、流式细胞术(FACS)分析人CXCR4在B16细胞中的表达,体内成瘤实验验证B16细胞的致瘤性。【结果】人CXCR4基因转染B16细胞,G418筛选获得阳性细胞克隆,RT-PCR检测到人CXCR4 mRNA的表达,流式细胞分析检测到人CXCR4蛋白的表达,体内成瘤实验证实异源CXCR4转染降低了B16的生长速度。【结论】异源CXCR4基因转染下调黑色素瘤的致瘤性,其机制可能与异源CXCR4诱导的免疫交叉反应有关。[Objective]To study the effect of xenogeneie ehemokine receptor CXCR4 gene transfeetion on tumorigeneeity of malignant tumors by transduetion of human CXCR4 gene into mouse melanoma B16 cells by use of gene transfer technology. [Methods]Liposome transfeetion assay was used to transduce human CXCR4 gene into mouse melanoma B16 cells. RT-PCR and FACS were selected to detect human CXCR4 expression in B16 cells. In vivo implantation experiments were used to study the tumorigenicity of B16 cells. [Results] G418-resistant clones were obtained after the transfeetion of B16 cells with human CXCR4 gene. And human CXCR4 transcript was detected by RT-PCR. The Results of FACS showed that B16 cells expressed human CXCR4 protein after the gene transfeetion. The tumor growth of B16 gene transfeetants was inhibited compared to the controls in in vivo experiments. [Conelusion]Xenogeneie CXCR4 transfeetion down-regulates the tumorigenicity of melanoma. The mechanism may be related to the induction of immune cross-reaction by xenogeneie gene transfer.
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