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为了研究生存素基因负性突变体生存素-D53A(SVV-D53A)对人肺腺癌SPC-A1移植瘤的治疗作用,并探讨其作用机制,我们在体外实验中使用SVV-D53A质粒转染人肺腺癌SPC-A1细胞,蛋白免疫印迹检测生存素突变体表达,同时通过流式细胞检测细胞凋亡情况。在体内实验中,裸鼠皮下接种人肺腺癌SPC-A1细胞建立肺癌移植瘤模型,使用阳离子脂质体包裹SVV-D53A质粒进行治疗。治疗结束后免疫组化检测各组肿瘤标本细胞增殖,末端脱氧核苷酸转移酶脱氧尿苷三磷酸切口末端标记(TUNEL)检测肿瘤细胞凋亡。与对照组相比,SVV-D53A质粒在体外显著诱导SPC-A1细胞凋亡,SVV-D53A组裸鼠皮下移植瘤体积减小,细胞增殖减弱,大量肿瘤细胞发生凋亡。研究结果表明SVV-D53A的表达在体外和体内均能够显著抑制人肺腺癌SPC-A1细胞的生长,其作用机制主要为诱导肿瘤细胞凋亡。
In order to investigate the therapeutic effect of Survivin-D53A (SVV-D53A), a negative mutant of survivin gene, on human lung adenocarcinoma SPC-A1 xenografts and its mechanism of action, we used SVV-D53A plasmid transfection in vitro The human lung adenocarcinoma SPC-A1 cells were detected by Western blotting, and the survivin mutant was detected by flow cytometry. In vivo experiments, nude mice were subcutaneously inoculated with human lung adenocarcinoma SPC-A1 cells to establish a lung cancer xenograft model, and the cationic liposomes were used to coat the SVV-D53A plasmid for treatment. At the end of treatment, the proliferation of tumor samples in each group was detected by immunohistochemistry. Apoptosis of tumor cells was detected by TUNEL. Compared with the control group, the SVV-D53A plasmid significantly induced the apoptosis of SPC-A1 cells in vitro. The volume of subcutaneous xenografts in SVV-D53A group was decreased, the cell proliferation was weakened, and a large number of tumor cells were apoptosis. The results show that the expression of SVV-D53A can significantly inhibit the growth of human lung adenocarcinoma SPC-A1 cells both in vitro and in vivo, and its mechanism of action is mainly to induce tumor cell apoptosis.