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Expression of bcl-2 in Burkitt's lymphoma cell lines: induction by latent
Epstein-Barr virus genes
J Finke, R Fritzen, P Ternes, P Trivedi, KJ Bross, W Lange, R Mertelsmann and G Dolken
Department of Hematology and Oncology, Medizinische Klinik, University of
Freiburg, Germany.
The bcl-2 oncogene blocks programmed cell death (apoptosis). Epstein- Barr
virus (EBV) can immortalize B lymphocytes into continuously growing
lymphoblastoid cell lines (LCL) by the coordinate expression of at least 9
latent genes (EBV nuclear antigen [EBNA] 1-6, latent membrane protein
[LMP], and terminal proteins [TP] 1 and 2). We analyzed transcription and
expression of bcl-2 and latent EBV genes in Burkitt's lymphoma (BL) cell
lines with a germinal center phenotype (group I) as well as activated BL
cell lines (group III) and LCLs. We found high expression of bcl-2 as well
as the full spectrum of latent EBV genes in LCLs and activated group III BL
cell lines. Group I BL cells expressed little or no bcl-2, EBNA-2, and LMP.
Superinfection with nondefective EBV or an EBNA-2-defective virus as well
as transfection with EBNA-2- or LMP-carrying vectors into the EBV-negative
cell lines RAMOS, DG75, U698, or BJAB induced upregulation of bcl-2
expression. The strongest effect on bcl-2 was obtained by transfection with
LMP, or infection with the nondefective virus. No change of bcl-2
expression was observed with EBNA-1. Our data indicate that the
immortalization capacity of EBV and the growth advantage of EBV- positive
compared with EBV-negative BL cells in vitro may predominantly be mediated
via induction of bcl-2 and the main effectors are EBNA-2 and LMP.
Volume 80,
Issue 2,
pp. 459-469,
07/15/1992
Copyright © 1992 by The American Society of Hematology
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