{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,19]],"date-time":"2025-10-19T18:16:28Z","timestamp":1760897788658},"reference-count":24,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T00:00:00Z","timestamp":1513900800000},"content-version":"vor","delay-in-days":8118,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Immunology &amp; Cell Biology"],"published-print":{"date-parts":[[1995,10]]},"abstract":"<jats:title>Summary<\/jats:title><jats:p>Epstein\u2010Barr virus (EBV) has been shown, in many instances, to protect B cells from apoptosis via expression of select EBV proteins and up\u2010regulation of bcl\u20102 or its homologues. However, at present little is known about the influence of EBV infection against cancer therapy\u2010induced apoptosis in EBV\u2010associated cancers. Many anti\u2010cancer treatments act via inhibition of protein synthesis and so could influence the reported protein\u2010dependent mechanisms involved in EBV inhibition of apoptosis. In the present study. Burkitt lymphoma (BJA\u2010B) cells were treated with a potent protein synthesis inhibitor, cycloheximide (CHX). Two variants of BJA\u2010B cells were used, one with EBV infection (EBV(+)), and one free of infection (EBV(\u2010)). Cells were collected 0, 3, 6, 12, 24 and 48 h after addition of either 1 or 50 \u03bcg\/mL of CHX. Control cultures were untreated. Apoptosis was quantified using established morphological and biochemical characteristics, and protein concentrations assessed. CHX treatment of EBV(\u2010) BJA\u2010B 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 EBV(\u2010) and EBV(+) cells is not dependent on new protein synthesis, and may be caused by removal of a \u2018cell survival\u2019 protein. In addition, the reduction in CHX\u2010induced apoptosis in the EBV(+) cells, when compared with similarly treated EBV(\u2010) cells, is not dependent on new protein synthesis and so may be indicative of a bcl\u20102 independent mechanism in this instance. The results have important implications for devising and assessing treatment of EBV\u2010associated malignancies.<\/jats:p>","DOI":"10.1038\/icb.1995.72","type":"journal-article","created":{"date-parts":[[2007,7,3]],"date-time":"2007-07-03T09:09:07Z","timestamp":1183453747000},"page":"463-468","source":"Crossref","is-referenced-by-count":9,"title":["Cycloheximide\u2010induced apoptosis in Burkitt lymphoma (BJA\u2010B) cells with and without Epstein\u2010Barr virus infection"],"prefix":"10.1111","volume":"73","author":[{"given":"HIDEAKI H","family":"ISHII","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"MARIA R","family":"ETHERIDGE","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"GLENDA C","family":"GOB\u00c9","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2017,12,22]]},"reference":[{"key":"e_1_2_1_2_2","doi-asserted-by":"publisher","DOI":"10.1038\/321653a0"},{"key":"e_1_2_1_3_2","doi-asserted-by":"publisher","DOI":"10.1126\/science.1659743"},{"key":"e_1_2_1_4_2","doi-asserted-by":"publisher","DOI":"10.1016\/0277-5379(91)90023-7"},{"key":"e_1_2_1_5_2","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.84.22.8060"},{"key":"e_1_2_1_6_2","doi-asserted-by":"publisher","DOI":"10.1002\/j.1460-2075.1988.tb02874.x"},{"key":"e_1_2_1_7_2","doi-asserted-by":"publisher","DOI":"10.1038\/349612a0"},{"key":"e_1_2_1_8_2","doi-asserted-by":"publisher","DOI":"10.1016\/0092-8674(91)90007-L"},{"key":"e_1_2_1_9_2","first-page":"2808","article-title":"Ultrastructural localization of BHRF1: an Epstein\u2010Barr virus gene product which has homology with bcl\u20102","volume":"54","author":"Hicktish T","year":"1994","journal-title":"Cancer Res."},{"key":"e_1_2_1_10_2","first-page":"5","volume-title":"Apoptosis: The Molecular Basis of Cell Death","author":"Kerr JFR","year":"1991"},{"key":"e_1_2_1_11_2","doi-asserted-by":"publisher","DOI":"10.1007\/BF00048057"},{"key":"e_1_2_1_12_2","doi-asserted-by":"publisher","DOI":"10.1038\/bjc.1991.341"},{"key":"e_1_2_1_13_2","doi-asserted-by":"publisher","DOI":"10.1080\/09553009214551481"},{"key":"e_1_2_1_14_2","first-page":"545","article-title":"Rapid induction of apoptosis in rat liver by ycloheximide","volume":"140","author":"Ledda\u2010Columbano GM","year":"1992","journal-title":"Am. 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