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人Ｐ５３基因位于１７ 号染色体短臂上（１７ｐ１３．１） ，编码一个由３９３ 个氨基酸组成的核磷酸蛋白，有调控细胞的生长，维持基因组的稳定，其突变、缺失在恶性肿瘤发生发展中起着非常重要的作用。为进一步探讨野生型Ｐ５３ 基因的抗肿瘤特性，我室采用分子克隆方法构建了重组野生型Ｐ５３ 真核表达载体（ｐｘＴ１—Ｐ５３） ，用磷酸钙—ＤＮＡ 共沉淀法将其导入人肝癌ＨｅｐＧ２ 细胞内，通过标记基因ＮｅＯＲ 筛选带外源Ｐ５３ 基因的Ｇ４１８ 抗药性克隆，对Ｇ４１８ 抗药性克隆细胞的生长增殖和粘附能力进行观察。结果表明，导入野生型Ｐ５３基因能使肝癌ＨｅｐＧ２ 细胞的生长增殖速度较对照细胞明显减慢，细胞粘附能力下降。提示野生型Ｐ５３ 基因能抑制肝癌细胞的生长。本研究为肝癌的Ｐ５３ 实验性基因治疗提供了一定的依据。
The human P53 gene is located on the short arm of chromosome 17 (17p13.1) and encodes a 393-amino-acid nucleoprotein that regulates cell growth and maintains genome stability. Its mutations and deletions play a role in the development of malignancies. It plays a very important role. To further explore the anti-tumor properties of wild-type P53 gene, a recombinant wild-type P53 eukaryotic expression vector (pxT1-P53) was constructed by molecular cloning method in our laboratory and was introduced into human liver cancer HepG-2 by calcium phosphate-DNA co-precipitation method. In the cells, G418 resistant clones carrying the exogenous P53 gene were screened by the marker gene NeOR to observe the growth, proliferation and adhesion ability of the G418 resistant clone cells. The results showed that the introduction of wild-type P53 gene can make the growth rate of hepatic carcinoma HepG 2 cells significantly slower than that of control cells, and the ability of cell adhesion decreased. It suggests that the wild-type P53 gene can inhibit the growth of hepatoma cells. This study provides a basis for the experimental gene therapy of P53 in liver cancer.