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目的腺病毒介导KDR启动子驱动的CDglyTK融合基因(AdKDRCDglyTK)体系对实体肿瘤细胞及血管内皮细胞靶向杀伤作用。方法分别将KDR和CMV启动子融合基因腺病毒体外感染表达KDR的ECV304、MCF7、MGC803及SW620细胞株和不表达KDR的LS174T细胞株,并给予不同浓度的前药5FC和/或GCV,观察其对各细胞株的杀伤效应及其旁观者效应。结果两种腺病毒对各细胞的感染率随腺病毒滴度的递增而增加,当MOI为200时,各细胞株均达约100%感染;感染AdCMVCDglyTK的各组细胞和感染AdKDRCDglyTK的ECV304、MCF7、MGC803及SW620对前药具有较高的敏感性,且其敏感性差异无统计学意义(P均>0.05);与其他细胞相比,感染AdKDRCDglyTK的LS174T细胞对前药不敏感(P<0.01);且观察到该体系明显的旁观者效应。结论KDR基因启动子调控的CDglyTK融合基因体系可选择性杀伤实体肿瘤细胞及血管内皮细胞。
Objective Adenovirus-mediated KDR promoter driven CDglyTK fusion gene (AdKDRCDglyTK) system on solid tumor cells and vascular endothelial cells targeted killing. Methods KDR-expressing ECV304, MCF7, MGC803 and SW620 cells and LS174T cells not expressing KDR were infected with KDR and CMV promoter fusion adenovirus in vitro and 5FC and / or GCV with different concentrations of KDR were observed respectively Killing effect on each cell line and its bystander effect. Results The infection rate of each adenovirus to each cell increased with the increase of adenovirus titer. When the MOI was 200, each cell line reached about 100% infection. The cells infected with AdCMVCDglyTK and the cells infected with AdKDRCDglyTK were ECV304, MCF7 , MGC803 and SW620 were highly sensitive to prodrugs, and their sensitivity was not statistically different (P> 0.05). Compared with other cells, LS174T cells infected with AdKDRCDglyTK were not sensitive to prodrug (P <0.01) ); And the apparent bystander effect was observed for this system. Conclusion CDglyTK fusion gene system regulated by KDR gene promoter can selectively kill solid tumor cells and vascular endothelial cells.