21 August 1997, Volume 15, Issue 8, Pages 971 – 980

Article

v-Rel prevents apoptosis in transformed lymphoid cells and blocks TNF-induced cell death Wei-Xing Zong1,2, Michael Farrell1,2, Judy Bash1,3 & Céline Gélinas1,4,5 1Center for Advanced Biotechnology and Medicine, University of Medicine and Dentistry of New Jersey     2Graduate Program in Biochemistry and Molecular Biology, University of Medicine and Dentistry of New Jersey     3Graduate Program in Microbiology and Molecular Genetics, Rutgers University     4Department of Biochemistry, and Cancer Institute of New Jersey, University of Medicine and Dentistry of New Jersey – Robert Wood Johnson Medical School, Piscataway, New Jersey 08854-5638, USA     5Author for correspondence

Keywords

v-Rel;   apoptosis;   cell transformation;   tetracycline-regulation

Abstract

The v-Rel oncoprotein belongs to the Rel/NF-B family of transcription factors. It transforms chicken lymphoid cells in vitro and induces fatal lymphomas in vivo. In this study, we used a tetracycline-regulated system to characterize the role of v-Rel in cell transformation. We show that the continued expression of v-Rel is necessary to maintain the viability of transformed lymphoid cells and enables primary spleen cells to escape apoptosis in vitro culture. In agreement with a possible role for v-Rel in the inhibition of programmed cell death, its inducible expression in HeLa cells prevented TNF-induced apoptosis. While the repression of v-Rel was accompanied by the rapid degradation of IB, changes in the steady-state levels of the apoptosis inhibitors Bcl-2 and Bcl-XL were only observed following the onset of cell death in transformed lymphoid cells. This suggests that the anti-apoptotic activity of v-Rel may affect other apoptosis inhibitors or other factors in the death pathway. Together, these findings demonstrate that v-Rel blocks apoptosis and suggest that this activity may be an important component of its transforming function.

Received 17 March, 97; Revised 9 May, 97; Accepted 9 May, 97

^© Macmillan Publishers Ltd 1997