Epstein-Barr virus growth/latency III program alters cellular microRNA expression

被引:123
作者
Cameron, Jennifer E. [1 ,2 ]
Fewell, Claire [3 ]
Yin, Qinyan [1 ,2 ,3 ]
McBride, Jane [3 ]
Wang, Xia [3 ]
Lin, Zhen [1 ,2 ,3 ]
Flemington, Erik K. [1 ,2 ,3 ]
机构
[1] Tulane Univ, Hlth Sci Ctr, Louisiana Canc Res Consortium, New Orleans, LA 70112 USA
[2] Tulane Univ, Hlth Sci Ctr, Tulane Canc Ctr, New Orleans, LA 70112 USA
[3] Tulane Univ, Hlth Sci Ctr, Dept Pathol, New Orleans, LA 70112 USA
基金
美国国家卫生研究院;
关键词
Epstein-Barr virus; EBV; miRNA; Microrna; Latency; miR-21; miR-23a cluster; miR-23a; miR-24; miR-27a; miR-28; miR-34a; miR-146; miR-155;
D O I
10.1016/j.virol.2008.09.018
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
The Epstein-Barr Virus (EBV) is associated with lymphoid and epithelial cancers. Initial EBV infection alters lymphocyte gene expression, inducing cellular proliferation and differentiation as the virus transitions through consecutive latency transcription programs. Cellular microRNAs (miRNAs) are important regulators of signaling pathways and are implicated in carcinogenesis. The extent to which EBV exploits cellular miRNAs is unknown. Using micro-array analysis and quantitative PCR, we demonstrate differential expression of cellular miRNAs in type III versus type I EBV latency including elevated expression of miR-21, miR-23a, miR-24, miR-27a, miR-34a, miR-146a and b, and miR-155. In contrast, miR-28 expression was found to be lower ill type III latency. The EBV-mediated regulation Of cellular miRNAs may contribute to EBV signaling and associated cancers. (C) 20108 Elsevier Inc. All rights reserved.
引用
收藏
页码:257 / 266
页数:10
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