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重组体，用电穿孔方法将其导入有ｐ５３基因突变的人肠癌ＳＷ１１１６细胞，通过标记基因ＮｅｏＲ筛选带外源ｐ５３基因的Ｇ４１８抗药性克隆，以观察抗药性克隆数量，同时对Ｇ４１８抗药性细胞的生长速度及细胞增殖周期进行观察，结果表明：导入ＷＴ—ｐ５３基因能使肠癌ＳＷ１１１６细胞的Ｇ４１８抗药性克隆形成减少，细胞生长速度较对照细胞明显减慢，细胞增殖周期Ｇ１期增加、Ｓ期下降。这些结果证明人野生型ｐ５３基因能抑制肠癌细胞的生长。本研究为大肠癌ＷＴ—ｐ５３实验性基因治疗提供了理论依据，说明基于恢复ｐ５３肿瘤抑制基因功能的基因治疗在治疗结直肠癌方面有着广阔的应用前景。
The recombinants were introduced into human colon cancer SW1116 cells with p53 gene mutation by electroporation, and G418 resistant clones with exogenous p53 gene were screened by the marker gene NeoR to observe the number of resistant colonies and G418 resistant cells at the same time. The growth rate and cell proliferation cycle were observed. The results showed that the introduction of WT-p53 gene can reduce the formation of G418 resistant clones in colon cancer SW1116 cells. The cell growth rate was significantly slower than that of the control cells, and the cell proliferation cycle G1 phase increased. Decline. These results demonstrate that the human wild-type p53 gene can inhibit the growth of colon cancer cells. This study provides a theoretical basis for WT-p53 experimental gene therapy for colorectal cancer, and demonstrates that gene therapy based on the function of restoring p53 tumor suppressor gene has a broad application prospect in the treatment of colorectal cancer.