[Effects of Epstein-Barr virus on host gene expression in Burkitt's lymphoma cell lines].

Peter Broderick, Michael Hubank, Alison Sinclair
{"title":"[Effects of Epstein-Barr virus on host gene expression in Burkitt's lymphoma cell lines].","authors":"Peter Broderick,&nbsp;Michael Hubank,&nbsp;Alison Sinclair","doi":"10.5732/cjc.009.10061","DOIUrl":null,"url":null,"abstract":"<p><strong>Background and objective: </strong>Epstein-Barr virus (EBV) is present in Burkitt's lymphoma (BL) cells in a latent form, showing a highly restricted pattern of gene expression with few tumor cells undergoing viral lytic replication. BL cell lines can be induced to enter the viral lytic cycle and initiate replication by stimulating surface immunoglobulin molecules. During this process many EBV genes are expressed that have the potential to influence host gene expression. We aimed to identify host genes that are regulated by EBV in BL cells and those that are regulated following ligation of surface IgG.</p><p><strong>Methods: </strong>The differentially expressed genes in EBV-positive Akata cells and EBV-negative AK31 cells were detected by microarray.</p><p><strong>Results: </strong>A total of 91 human genes were differentially expressed between Akata and AK31 cells and 198 were differentially expressed when cells were stimulated to enter lytic replication. The differential expression of one gene, myd88, was correlated with disrupted TLR9 signaling.</p><p><strong>Conclusions: </strong>EBV down-regulates most of the genes regulated by surface Ig cross-linking in the early stages of lytic cycle activation. These include genes involved in cell survival, signal transduction, transcription control and the immune response that may mediate EBV transformation of B-lymphocytes and others such as HDAC4 that may affect virus replication.</p>","PeriodicalId":7559,"journal":{"name":"Ai zheng = Aizheng = Chinese journal of cancer","volume":" ","pages":"813-21"},"PeriodicalIF":0.0000,"publicationDate":"2009-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Ai zheng = Aizheng = Chinese journal of cancer","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.5732/cjc.009.10061","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0

Abstract

Background and objective: Epstein-Barr virus (EBV) is present in Burkitt's lymphoma (BL) cells in a latent form, showing a highly restricted pattern of gene expression with few tumor cells undergoing viral lytic replication. BL cell lines can be induced to enter the viral lytic cycle and initiate replication by stimulating surface immunoglobulin molecules. During this process many EBV genes are expressed that have the potential to influence host gene expression. We aimed to identify host genes that are regulated by EBV in BL cells and those that are regulated following ligation of surface IgG.

Methods: The differentially expressed genes in EBV-positive Akata cells and EBV-negative AK31 cells were detected by microarray.

Results: A total of 91 human genes were differentially expressed between Akata and AK31 cells and 198 were differentially expressed when cells were stimulated to enter lytic replication. The differential expression of one gene, myd88, was correlated with disrupted TLR9 signaling.

Conclusions: EBV down-regulates most of the genes regulated by surface Ig cross-linking in the early stages of lytic cycle activation. These include genes involved in cell survival, signal transduction, transcription control and the immune response that may mediate EBV transformation of B-lymphocytes and others such as HDAC4 that may affect virus replication.

查看原文
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
eb病毒对伯基特淋巴瘤细胞系宿主基因表达的影响
背景和目的:eb病毒(EBV)以潜伏形式存在于伯基特淋巴瘤(BL)细胞中,表现出高度受限的基因表达模式,很少有肿瘤细胞进行病毒裂解复制。通过刺激表面免疫球蛋白分子,可以诱导BL细胞系进入病毒裂解周期并开始复制。在这个过程中,许多EBV基因的表达有可能影响宿主基因的表达。我们的目的是鉴定在BL细胞中受EBV调控的宿主基因和在表面IgG结扎后受调控的宿主基因。方法:采用芯片检测ebv阳性Akata细胞和ebv阴性AK31细胞的差异表达基因。结果:共有91个人类基因在Akata和AK31细胞中差异表达,其中198个基因在刺激细胞进入裂解复制时差异表达。myd88基因的差异表达与TLR9信号通路中断有关。结论:EBV在裂解周期激活的早期阶段下调了大部分受表面Ig交联调控的基因。这些基因包括参与细胞存活、信号转导、转录控制和免疫反应的基因,这些基因可能介导eb病毒在b淋巴细胞中的转化,以及其他可能影响病毒复制的基因,如HDAC4。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 去求助
来源期刊
自引率
0.00%
发文量
0
期刊最新文献
[Vascular endothelial growth factor (VEGF)-D in association with VEGF receptor-3 in lymphatic metastasis of breast cancer]. [Correlation of the sensitivity of NP chemotherapy in non-small lung cancer with DNA repair gene XRCC1 polymorphism]. [Correlation of hypermethylation of TSP1 gene with TGF-beta1 level and T cell immunity in gastric cardia adenocarcinoma]. [Efficacy and survival of 92 cases of Ewing's sarcoma family of tumor initially treated with multidisciplinary therapy]. [Clinical characteristics and prognosis of very young patients with breast cancer in the southern of China].
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1