Abstract
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. Key words: Carcinoma,hepatocellular; p53; S-adenosylmethionine; GADD45β; Promoter
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