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Falk, M.H. ; Hültner, L. ; Milner, A.E. ; Gregory, C.D. ; Bornkamm, G.W.

Irradiated fibroblasts protect Burkitt lymphoma cells from apoptosis by a mechanism independent of BCL-2.

Int. J. Cancer 55, 485-491 (1993)
DOI
Open Access Green as soon as Postprint is submitted to ZB.
When cells of fresh Burkitt lymphoma (BL) biopsies are explanted into tissue culture, their survival and groth are greatly dependent on the presence of a feeder layer of irradiated fibroblasts. To investigate the nature of this feeder dependence, we characterized the growth requirements of a panel of Epstein-Barr Virus (EBV)-negative and -positive BL cell lines in both the absence and the presence of feeder clels in vitro. Four EBV-negative BL lines and 4 EBV-positive lines displaying the phenotype of BL cells in vivo required high cell density for proliferation in the absence of feeder cells, but grew out as single-cell clones when seeded on irradiated human fibroblasts. EBV-positive BL cell lines which had acquired an activated phenotype similar to that of lymphoblastoid cell lines required much lower cell densities for autonomous proliferation. The EBV-negative Burkitt lymphoma line BL70 was used as a model to study the feeder-cell dependence in more detail. BL70 cells grew in the absence of feeder cells only at high cell density and at high FCS concentration. In the presence of feeder cells, BL70 cells became clonogenic even at greatly reduced FCS concentration. A decrease in either cell density or FCS concentration induced apoptosis. Supernatants from feeder cells and from BL70 cells growing autonomously at high cell density were unable to substitute for the survival and growth-promoting effect of the feeder cells. Protection of Burkitt lymphoma cells from apoptosis by co-cultivation with irradiated fibroblasts was not mediated by induction of bcl-2. The system described here may be relevant for the in vivo situation since Burkitt lymphoma cells are protected from c-MYC induced apoptosis in vivo also by a mechanism which does not involve bcl-2.
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Publication type Article: Journal article
Document type Scientific Article
Corresponding Author
ISSN (print) / ISBN 0020-7136
e-ISSN 1097-0215
Journal International Journal of Cancer
Quellenangaben Volume: 55, Issue: 3, Pages: 485-491 Article Number: , Supplement: ,
Publisher Wiley
Non-patent literature Publications
Reviewing status Peer reviewed
Institute(s) Institute of Clinical Molecular Biology and Tumor Genetics (K.MOLBI)