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Burkitt's lymphoma cells are resistant to programmed cell death in the presence of the epstein‐barr virus latent antigen EBNA‐4
Author(s) -
Silins Sharon L.,
Sculley Tom B.
Publication year - 1995
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/ijc.2910600110
Subject(s) - programmed cell death , apoptosis , lymphoma , biology , germinal center , virus , antigen , epstein–barr virus , cell culture , phenotype , b cell , cancer research , immunology , virology , gene , antibody , genetics
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 1 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. © 1995 Wiley‐Liss, Inc.