抑癌基因p1 6和 p53在抑制肿瘤的发生中起重要作用 ,在髓细胞白血病细胞系K562中检测出这两种基因有纯合缺失。为探讨野生型 p1 6和 p53基因的转染与表达对K562细胞的生长影响 ,采用了脂质体介导外源野生型 p1 6和 p53共转染K562细胞 ,用免疫细胞化学染色检测p1 6和 p53基因的表达 ,检测细胞生长曲线 ,采用流式细胞术进行细胞周期分析。结果显示 ,共转染后 p53和p1 6在K562细胞中表达阳性率分别为 2 3 %和 2 8% ;细胞生长受到一定程度的抑制 ,G1 期细胞的比例增加 ,S期细胞减少 ,与单独转染 p53或p1 6基因的抑制作用有明显差别 (P <0 .0 5)。结论 :外源野生型 p1 6和p53基因的共转染比转染单基因对K562细胞生长有更明显的抑制作用 ,有可能成为白血病基因治疗的一种方法 Tumor suppressor genes p1 6 and p53 play an important role in tumorigenesis inhibition. In myeloid leukemia cell line K562, there was a loss of homozygosity for both genes. To investigate the effect of wild-type p1 6 and p53 gene transfection and expression on the growth of K562 cells, liposome-mediated exogenous wild-type p1 6 and p53 co-transfected K562 cells, immunocytochemical staining for p16 And p53 gene expression, detection of cell growth curve, the use of flow cytometry cell cycle analysis. The results showed that the positive rates of p53 and p16 expression in K562 cells were 23% and 28% respectively after co-transfection; the cell growth was inhibited to a certain extent, the proportion of cells in G1 phase increased and the number of S phase cells decreased, The inhibition of p53 or p1 6 gene transfection was significantly different (P <0.05). CONCLUSION: Co-transfection of exogenous wild-type p1 6 and p53 gene can significantly inhibit the growth of K562 cells compared with transfection of single gene and may be a method of gene therapy for leukemia