Abstract
Group I Epstein-Barr virus (EBV)-positive Burkitt's lymphoma (BL) cells display a surface phenotype characteristic of germinal centre B cells and readily undergo apoptosis in response to a variety of stimuli, including serum deprivation. Activation of EBV latent gene expression has been shown to increase the survival of these tumour cells by blocking programmed cell death. To investigate the nature of this protection, we assessed the function of the EBV latent EBNA-4 gene in a group I lymphoma line, dG75. Group I BL cells induced to undergo apoptosis in response to serum starvation were protected in the presence of EBNA-4 protein. A possible factor underlying this EBNA-4-associated survival was increased expression of the oncoprotein bcl-2, a known repressor of cell death. Together these data suggest that EBNA-4 plays an important role in the regulation of programmed cell death in BL tumour cells.
Publication types
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Comparative Study
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Animals
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Antigens, Viral / genetics
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Antigens, Viral / physiology*
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Apoptosis / physiology*
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Burkitt Lymphoma / genetics
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Burkitt Lymphoma / pathology*
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Burkitt Lymphoma / virology*
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Callithrix
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Cell Death / physiology
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Cell Division / physiology
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Cell Survival / physiology
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DNA, Neoplasm / analysis
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DNA-Binding Proteins / genetics
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DNA-Binding Proteins / physiology*
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Epstein-Barr Virus Nuclear Antigens
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Gene Expression Regulation, Neoplastic
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Herpesvirus 4, Human / genetics*
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Herpesvirus 4, Human / immunology*
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Oncogenes
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Proto-Oncogene Proteins / genetics
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Proto-Oncogene Proteins c-bcl-2
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Transfection
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Tumor Cells, Cultured
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Up-Regulation / physiology
Substances
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Antigens, Viral
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DNA, Neoplasm
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DNA-Binding Proteins
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Epstein-Barr Virus Nuclear Antigens
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Proto-Oncogene Proteins
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Proto-Oncogene Proteins c-bcl-2