野生型p16和p53抑癌基因共转染对 K562细胞增殖的抑制作用

抑癌基因p16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p16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p16和p53共转染K562细胞，用免疫细胞化学染色检测p16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p16在K562细胞中表达阳性率分别为23％和28％；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p16基因的抑制作用有明显差别(P＜0.05)。结论：外源野生型p16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。

Inhibition of K562 Cell Proliferation by Wild Type p16 and p53 Genes Cotransfection

The tumor suppressor gene p53 and p16, both of which play an important role in inhibition of tumorigenesis, are homozygously deleted in human myeloid leukemia cell line K562. To explore the inhibition of K562 cell proliferation by wild type p16 and p53 genes, both p16 and p53 genes were co-transfected into K562 cells mediated by liposome. The expression of the two genes was measured by immunocytochemical method, the cell cycle was analysed by flow cytometry, and the number of recovered viable cells was assessed after transfection. After co-transfection, the p53 and p16 positive cells were 23% and 28%, respectively. The results showed that co-transfection of p16 and p53 genes significantly inhibits cell proliferation comparing with transfection either by p16 gene or by p53 gene (P < 0.05). Expression of p16 and p53 proteins increased the cell number in G(1) phase but decreased the cell number in S phase. It is concluded that co-transfection of p16 and p53 genes has a stronger growth-inhibitory effect on K562 cell growth than that of transfection only by p16 gene or by p53 gene, may be a pathway for gene therapy in leukemia.