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目的：构建ｐ５３表达质粒，研究ｐ５３基因对白血病细胞Ｋ５６２细胞生长的抑制作用。方法：以Ｔ４连接酶把２１６０ｂｐ的ｐ５３ｃＤＮＡ片段插入ｐＲｃ／ＣＭＶ质粒，重组构建ｐＲｃ／ｐ５３表达质粒，以Ｌｉｐｏｆｅｃｔｉｎ介导ｐＲｃ／ｐ５３质粒转染Ｋ５６２细胞，以甲基纤维素半固体培养方法作Ｋ５６２细胞体外克隆培养，观察转染ｐ５３基因后Ｋ５６２细胞克隆形成改变。结果：ｐ５３ｃＤＮＡ质粒转染的Ｋ５６２细胞，体外培养克隆形成能力明显减低。在接种１×１０４细胞时，未转染的空白对照组及空质粒对照组白血病细胞集落数分别是２７９７±２６４和２７２５±２６１；而ｐ５３质粒转染组细胞集落数是１０６１±１６０；与空质粒转染组及未转染的Ｋ５６２细胞组比较有非常显著性差异（Ｐ＜０００１，ｎ＝１０）。结论：转染ｐ５３基因能抑制Ｋ５６２细胞的生长。
OBJECTIVE: To construct the p53 expression plasmid and study the inhibitory effect of p53 gene on the growth of leukemia K562 cells. METHODS: The 2160bp p53 cDNA fragment was inserted into pRc / CMV plasmid by T4 ligase and the pRc / p53 expression plasmid was constructed. The K562 cells were transfected with pRc / p53 plasmids by Lipofectin and K562 cells were treated by methylcellulose semi-solid culture In vitro cloning and culture, observed after transfection of p53 gene K562 cell clone formation changes. RESULTS: K562 cells transfected with p53 cDNA plasmid had a significantly lower ability to form clones in vitro. The number of leukemic cells in untransfected blank control group and empty plasmid control group were 2797 ± 264 and 2725 ± 261 respectively when inoculated with 1 × 104 cells, while the number of cell colonies in transfected group was 1061 ± 160; There was a significant difference between plasmid transfection group and untransfected K562 cells (P <0001, n = 10). Conclusion: Transfection of p53 gene can inhibit the growth of K562 cells.