中文摘要：

目的 观察p53对肝癌细胞GADD45β诱导的影响并探讨其机制.方法 转染p53全序列建立Hep3B^＋p53;比较S腺苷蛋氨酸对Hep3B^＋p53的GADD45β表达诱导及其对近端启动子活性影响;比较DNA合成能力和细胞克隆形成能力及其对Caspase基因的影响.结果 Hep3B^＋p53可以稳定表达p53蛋白;p53转染能使S腺苷蛋氨酸对Hep3B^＋p53中GADD45β的表达诱导由0.0089增加至0.0192和0.0371,同时使启动子中3个核因子（NF）-κB活性分别增强1倍、50%和25%,Hep3B^＋p53的DNA合成能力降至80.99%和42.53%,细胞克隆形成能力的抑制率为15.04%和90.42%;Hep3B^＋p53的Caspase-8、Caspase-9和Caspase-3的活性无明显变化.结论 p53在肝癌细胞的GADD45β表达诱导中有重要作用,增强转录调节因子的表达水平是其可能的作用机制.

英文摘要：

Objective To identify the role of p53 in the induction of GADD45β in HCC cells. Methods Hep3B^＋p53 clone was established by the transfection of the full-length p53 sequence to Hep3B. Following S-adenesylmethionine administration, quantitative real-time PCR were employed to validate the expression changes of GADD45β. pGL3 basic lucfferase plasmids including promoter fragments were synthesized in vitro and transfected into cells. The effects on promoter activity, cell growth and the expression of Caspase were further focused on. Results Hep3B^＋p53 could express p53 protein stably. The transfection of p53 could enhance the induction of GADD45β in Hep3B by S-adenosylmethionine. The promoter activity of fragments constructing NF-κB binding sites could be induced by transfection of p53. The colony formation and DNA syntheses were inhibited apparently in Hep3B^＋p53 with p53 by S-adenosylmethionine. However, the p53 transfection could not influence the cleavage of Caspases. Conclusion p53 may play a role in the induction of GADD45β in Hep3B, which may result from the regulation of transcription factors in proximal promoter.