Abstract
X gene product of hepatitis B virus (HBV) (HBx) regulates many transcription factors including nuclear factor kappa B (NF-kappaB) and plays a key role in hepatocarcinogenesis. In this study, we demonstrated that the expression of full HBV genome and HBx gene similarly stimulated the transcriptional activity of NF-kappaB in HuH-7 human hepatoma cells, and that interferon (IFN)-alpha as well as dominant negative mutant of IkappaB kinase-alpha effectively inhibited the HBx-mediated NF-kappaB activation, but IFN-gamma did not. These results suggest that IFN-alpha may have a function to block the NF-kappaB activating pathway triggered by HBx in HBV hepatocytes.
MeSH terms
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Carcinoma, Hepatocellular / genetics
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Carcinoma, Hepatocellular / metabolism*
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Carcinoma, Hepatocellular / virology
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Genetic Vectors / metabolism
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Genome, Viral
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Hepatitis B virus / genetics
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Hepatitis B virus / metabolism*
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Humans
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I-kappa B Kinase
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Interferon-alpha / pharmacology*
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Liver Neoplasms / genetics
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Liver Neoplasms / metabolism*
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Liver Neoplasms / virology
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Luciferases / genetics
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NF-kappa B / antagonists & inhibitors*
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NF-kappa B / metabolism
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Protein Serine-Threonine Kinases / genetics
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Protein Serine-Threonine Kinases / metabolism
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Protein Serine-Threonine Kinases / pharmacology
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Trans-Activators / biosynthesis
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Trans-Activators / genetics
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Trans-Activators / physiology*
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Transcriptional Activation / physiology
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Transfection
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Tumor Cells, Cultured
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Viral Regulatory and Accessory Proteins
Substances
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Interferon-alpha
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NF-kappa B
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Trans-Activators
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Viral Regulatory and Accessory Proteins
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hepatitis B virus X protein
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Luciferases
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Protein Serine-Threonine Kinases
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CHUK protein, human
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I-kappa B Kinase
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IKBKB protein, human
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IKBKE protein, human