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[Interaction effect of p53 with HBV in hepatoma cell line SMMC-7721].

AbstractOBJECTIVES:
To study the interaction of hepatitis virus B (HBV) and tumor suppressor p53.
METHODS:
Plasmid pCMVp53 was transfected or cotransfected with pCMVHBVa (wild type HBV) or PCMVHBVb (mutant type HBV) into the hepatoma cell line SMMC-7721 by lipofectamine. Apoptosis cells were labeled by annexin V-FITC and confirmed by flow cytometry. Reporter plasmids PG13-CAT or p21-luc were cotransfected respectively in each group to indicate transactivation activity of p53 and it's effect on p21 promoter. Western blot was performed to observe p53 expression in each group.
RESULTS:
The group transfected by pCMVp53 alone exhibit higher luciferase activity and higher apoptosis rate, otherwise, p53 expression, enzyme activity of PG13-CAT or p21- luc and cell apoptosis rate were much higher in the group cotransfected by pCMVp53 and pCMVHBVa, but not in the other cotransfected group; HBV replication was enhanced in p53 cotransfected group.
CONCLUSION:
p53 expression and effects could be enhanced by HBV and p53 had positive regulation effect on HBV replication.
AuthorsJian-Hui Qu, Ming-Hua Zhu, Jing Lin, Can-Rong Ni, Fang-Mei Li, Zhi Zhu, Guan-Zhen Yu
JournalZhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology (Zhonghua Gan Zang Bing Za Zhi) Vol. 12 Issue 7 Pg. 403-5 (Jul 2004) ISSN: 1007-3418 [Print] China
PMID15268803 (Publication Type: English Abstract, Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Trans-Activators
  • Tumor Suppressor Protein p53
  • Luciferases
  • HRAS protein, human
  • Proto-Oncogene Proteins p21(ras)
Topics
  • Apoptosis
  • Carcinoma, Hepatocellular (genetics, pathology, virology)
  • Cell Line, Tumor
  • Hepatitis B virus (genetics, physiology)
  • Humans
  • Liver Neoplasms (genetics, pathology, virology)
  • Luciferases (metabolism)
  • Promoter Regions, Genetic
  • Proto-Oncogene Proteins p21(ras) (genetics)
  • Trans-Activators (genetics)
  • Transfection
  • Tumor Suppressor Protein p53 (genetics, metabolism)
  • Virus Replication

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