Journal Article

Oltipraz, a novel inhibitor of hepatitis B virus transcription through elevation of p53 protein.

W J Chi, S L Doong, S Y Lin-Shiau, C W Boone, G J Kelloff and J K Lin

in Carcinogenesis

Volume 19, issue 12, pages 2133-2138
Published in print December 1998 | ISSN: 0143-3334
Published online December 1998 | e-ISSN: 1460-2180 | DOI:
Oltipraz, a novel inhibitor of hepatitis B virus transcription through elevation of p53 protein.

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Molecular epidemiological studies of populations at high risk for liver cancer have shown that hepatitis B virus (HBV) and aflatoxin B1 exposures are two major risk factors for this disease. Oltipraz is currently being considered for clinical trial to protect against aflatoxin B1-induced hepatocarcinogenesis based on its proven protective effect in many different animal models. In addition, oltipraz inhibits human immunodeficiency virus (HIV) replication. The inactivation of reverse transcriptase of HIV appears to be the antiviral mechanism. It has been demonstrated that a number of compounds that inhibit HIV replication also inhibit HBV replication in vitro. Therefore, we tested the possibility of oltipraz blocking HBV replication in 2.2.15 cells (clonal cells derived from HepG2 cells that were transfected with a plasmid containing HBV DNA) in vitro. Results of the experiments indicate that oltipraz has a dose-dependent inhibitory effect on HBV replication and specifically blocks HBV transcription in 2.2.15 cells. In addition, oltipraz induces endogenous wild-type p53 protein in a dose- and time-course-dependent manner. Taken together, we speculate that the effects of oltipraz against replication of HBV and specific blocking of HBV transcription may be through the induction of p53-mediated pathway in 2.2.15 cells. In addition to its known chemopreventive action on aflatoxin B1 hepatocarcinogenesis, oltipraz was shown here to inhibit HBV replication. These dual effects put oltipraz as the excellent candidate for the chemopreventive agent of human hepatocellular carcinoma.

Journal Article.  0 words. 

Subjects: Clinical Cytogenetics and Molecular Genetics

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