论文部分内容阅读
目的：研究野生型ｐ５３基因对人肝癌细胞系细胞凋亡的作用。方法：通过脂质体转染方法将野生型ｐ５３基因（ｗｔ－ｐ５３）导入ｐ５３缺陷的ＨＣＣ－９２０４细胞系中，并获稳定表达。结果：转染ｗｔ－ｐ５３后细胞生长缓慢，Ｇ１期细胞数量由转基因前的４８．５％增加到７８．０％，并有较多细胞逐渐死亡。电镜观察和ＤＮＡ分析证实细胞死亡方式主要是细胞凋亡。免疫组化结果显示细胞转染ｗｔ－ｐ５３后，ｐ２１ＷＡＦ１／ＣＩＰ１的表达显著增加。结论：提示外源性野生型ｐ５３基因可以抑制肝癌细胞生长，并诱导细胞凋亡，这可能是通过ｐ２１ＷＡＦ１／ＣＩＰ１途径发挥上述作用的
Objective: To study the effect of wild-type p53 gene on apoptosis in human hepatoma cell lines. METHODS: The wild-type p53 gene (wt-p53) was introduced into the p53-defective HCC-9204 cell line by liposome transfection and was stably expressed. RESULTS: After transfection with wt-p53, the cells grew slowly. The number of cells in G1 phase increased from 48.5% before transgene to 78.0%, and more cells gradually died. Electron microscopy and DNA analysis confirmed that cell death was mainly apoptosis. The results of immunohistochemistry showed that the expression of p21WAF1/CIP1 was significantly increased after transfection of wt-p53 cells. Conclusion: It is suggested that exogenous wild-type p53 gene can inhibit the growth of hepatoma cells and induce apoptosis, which may be exerted by the p21WAF1/CIP1 pathway.