Cycloheximide-induced apoptosis in Burkitt lymphoma (BJA-B) cells with and without Epstein-Barr virus infection

Immunology and Cell Biology
H H IshiiG C Gobé

Abstract

Epstein-Barr virus (EBV) has been shown, in many instances, to protect B cells from apoptosis via expression of select EBV proteins and up-regulation of bcl-2 or its homologues. However, at present little is known about the influence of EBV infection against cancer therapy-induced apoptosis in EBV-associated cancers. Many anti-cancer treatments act via inhibition of protein synthesis and so could influence the reported protein-dependent mechanisms involved in EBV inhibition of apoptosis. In the present study, Burkitt lymphoma (BJA-B) cells were treated with a potent protein synthesis inhibitor, cycloheximide (CHX). Two variants of BJA-B cells were used, one with EBV infection (EBV(+)), and one free of infection (EBV(-)). Cells were collected 0,3,6,12, 24 and 48 h after addition of either 1 or 50 micrograms/mL of CHX. Control cultures were untreated. Apoptosis was quantified using established morphological and biochemical characteristics, and protein concentrations assessed. CHX treatment of EBV(-) BJA-B cells induced massive levels of apoptosis. Apoptosis was inhibited, but remained significantly higher than that found in control cultures, in similarly treated EBV(+) cells. The study demonstrates that induction of apoptosis in ...Continue Reading

References

Sep 1, 1992·Cancer Metastasis Reviews·J A Hickman
Oct 21, 1992·International Journal of Cancer. Journal International Du Cancer·A E MilnerC D Gregory
Sep 1, 1992·Cancer Metastasis Reviews·G P Owens, J J Cohen
Nov 22, 1991·Science·H zur Hausen
Jan 1, 1991·European Journal of Cancer : Official Journal for European Organization for Research and Treatment of Cancer (EORTC) [and] European Association for Cancer Research (EACR)·C PedersenE Ralfkiaer
Feb 1, 1991·International Journal of Radiation Biology·B V HarmonG C Gobé
Nov 1, 1987·Proceedings of the National Academy of Sciences of the United States of America·A CalenderG M Lenoir
Aug 1, 1993·Journal of Cellular Physiology·J Perreault, R Lemieux

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Citations

Sep 21, 2000·Transplantation Proceedings·Z RancewiczL Paczek
Jan 9, 2004·Journal of Toxicology and Environmental Health. Part a·Rebecca L Uzarski, James J Pestka
Jul 12, 2013·The Journal of Biological Chemistry·Chun-Ling DaiCheng-Xin Gong
Nov 11, 1999·Oncogene·M S Sheikh, A J Fornace
Nov 28, 2001·São Paulo Medical Journal = Revista Paulista De Medicina·C E KlumbR C Maia

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