Resistance to TGF-β1 correlates with a reduction of TGF-β type II receptor expression in Burkitt’s lymphoma and Epstein–Barr virus-transformed B lymphoblastoid cell lines

Inman, G. J. and Allday, M. J. (2000) Resistance to TGF-β1 correlates with a reduction of TGF-β type II receptor expression in Burkitt’s lymphoma and Epstein–Barr virus-transformed B lymphoblastoid cell lines. Journal of General Virology, 81(6), pp. 1567-1578. (doi:10.1099/0022-1317-81-6-1567) (PMID:10811940)

Inman, G. J. and Allday, M. J. (2000) Resistance to TGF-β1 correlates with a reduction of TGF-β type II receptor expression in Burkitt’s lymphoma and Epstein–Barr virus-transformed B lymphoblastoid cell lines. Journal of General Virology, 81(6), pp. 1567-1578. (doi:10.1099/0022-1317-81-6-1567) (PMID:10811940)

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Abstract

The pleiotropic cytokine TGF-β1 is a member of a large family of related factors involved in controlling cell proliferation, differentiation and apoptosis. TGF-β ligands interact with a complex of type I and type II transmembrane serine/threonine kinases and they transmit their signals to the nucleus via a family of Smad proteins. A panel of over 20 Burkitt’s lymphoma (BL) cell lines has been compiled including those that are Epstein–Barr virus (EBV) negative, those that carry EBV with a restricted pattern of EBV latent gene expression (group I) and those that express the full range of latent EBV genes (group III), together with selected EBV-transformed lymphoblastoid cell lines (LCLs). Most of the EBV-negative and group I BL cell lines underwent apoptosis or a G1 arrest in response to TGF-β1 treatment. In contrast, group III cell lines and LCLs were completely refractory to these effects of TGF-β1. All of the cell lines expressed the TGF-β pathway Smads and the TGF-β type I receptor. Lack of responsiveness to TGF-β1 appears to correlate with a down-regulation of TGF-β type II receptor expression. Studies of EBV-converted and stably transfected BL cell lines demonstrated that the EBV gene LMP-1 is neither necessary nor sufficient to block the TGF-β1 response.

Item Type:Articles
Additional Information:This work was supported by Wellcome Trust project grants 047383 and 050096 to M.J.A.
Status:Published
Refereed:Yes
Glasgow Author(s) Enlighten ID:Inman, Professor Gareth
Authors: Inman, G. J., and Allday, M. J.
College/School:College of Medical Veterinary and Life Sciences > Institute of Cancer Sciences
Journal Name:Journal of General Virology
Publisher:Microbiology Society
ISSN:0022-1317
ISSN (Online):1465-2099

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