Abstract
The expression of the cellular gene coding for the epidermal growth factor (EGF) receptor (EGF-R) was assayed in the presence of hepatitis B virus (HBV) gene expression under different experimental conditions in human hepatoma-derived cells. First, transfection experiments of the well-differentiated HepG2 human hepatoma cell line using different expression vectors of the HBV X-region demonstrated that the X-gene product is capable of inducing EGF-R gene overexpression; in addition, by using a stable in vitro expression system for HBV, it was shown that EGF-R gene expression in these cells is greater than in the uninfected parent cells, and that this results in a three-fold increase in 125I-EGF binding. Finally, a CAT-expression assay was performed, indicating that regulatory regions of the EGF-R-gene are target sequences for X-protein trans-activation.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Carcinoma, Hepatocellular / genetics
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Chloramphenicol O-Acetyltransferase / biosynthesis
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Chloramphenicol O-Acetyltransferase / genetics
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Epidermal Growth Factor / metabolism
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ErbB Receptors / biosynthesis
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ErbB Receptors / genetics*
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Genetic Vectors / genetics
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Hepatitis B virus / growth & development
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Humans
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Liver Neoplasms / genetics
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Promoter Regions, Genetic / genetics*
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Recombinant Fusion Proteins / biosynthesis
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Regulatory Sequences, Nucleic Acid / genetics
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Trans-Activators / genetics*
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Transcriptional Activation*
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Transfection / genetics
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Tumor Cells, Cultured
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Viral Regulatory and Accessory Proteins
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Virus Replication
Substances
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Recombinant Fusion Proteins
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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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Epidermal Growth Factor
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Chloramphenicol O-Acetyltransferase
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ErbB Receptors