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Animal: DNA Viruses |
1 correlates with a reduction of TGF- type II receptor expression in Burkitt’s lymphoma and Epstein–Barr virus-transformed B lymphoblastoid cell lines
Section of Virology and Cell Biology and the Ludwig Institute for Cancer Research, Imperial College of Science, Technology and Medicine, St Mary’s Campus, Norfolk Place, London W2 1PG, UK1
Author for correspondence: Martin Allday. Fax +44 20 7724 8586. e-mail m.allday{at}ic.ac.uk
The pleiotropic cytokine TGF-
1 is a member of a large family of related factors involved in controlling cell proliferation, differentiation and apoptosis. TGF- 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-1 treatment. In contrast, group III cell lines and LCLs were completely refractory to these effects of TGF-1. All of the cell lines expressed the TGF- pathway Smads and the TGF- type I receptor. Lack of responsiveness to TGF-1 appears to correlate with a down-regulation of TGF- 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-1 response.
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