Home | Help | Feedback | Subscriptions | Archive | Search | Latest Articles

This Article Full Text Full Text (PDF, 1502K) PPT slides of all figures Supplemental Material Index Alert me when this article is cited Citation Map Services Email this article Similar articles in this journal Similar articles in PubMed Alert me to new content in the JEM Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Choy, E. Y.-W. Articles by Jin, D.-Y. Search for Related Content PubMed PubMed Citation Articles by Choy, E. Y.-W. Articles by Jin, D.-Y. Social Bookmarking                      What's this?

¹ Department of Biochemistry, ² Department of Anatomy, and ³ Department of Clinical Oncology, The University of Hong Kong, Pokfulam, Hong Kong
⁴ Department of Anatomical and Cellular Pathology, State Key Laboratory in Oncology in South China, Li Ka Shing Institute of Health Science, Prince of Wales Hospital, Chinese University of Hong Kong, Shatin, New Territories, Hong Kong

CORRESPONDENCE Dong-Yan Jin: dyjin{at}hkucc.hku.hk

Epstein-Barr virus (EBV) is a herpesvirus associated with nasopharyngeal carcinoma (NPC), gastric carcinoma (GC), and other malignancies. EBV is the first human virus found to express microRNAs (miRNAs), the functions of which remain largely unknown. We report on the regulation of a cellular protein named p53 up-regulated modulator of apoptosis (PUMA) by an EBV miRNA known as miR-BART5, which is abundantly expressed in NPC and EBV-GC cells. Modulation of PUMA expression by miR-BART5 and anti–miR-BART5 oligonucleotide was demonstrated in EBV-positive cells. In addition, PUMA was found to be significantly underexpressed in 60% of human NPC tissues. Although expression of miR-BART5 rendered NPC and EBV-GC cells less sensitive to proapoptotic agents, apoptosis can be triggered by depleting miR-BART5 or inducing the expression of PUMA. Collectively, our findings suggest that EBV encodes an miRNA to facilitate the establishment of latent infection by promoting host cell survival.

© 2008 Choy et al. This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.jem.org/misc/terms.shtml). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 3.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/3.0/).

CiteULike    Complore    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this?

This article has been cited by other articles:

• Shannon-Lowe, C., Adland, E., Bell, A. I., Delecluse, H.-J., Rickinson, A. B., Rowe, M. (2009). Features Distinguishing Epstein-Barr Virus Infections of Epithelial Cells and B Cells: Viral Genome Expression, Genome Maintenance, and Genome Amplification. J. Virol. 83: 7749-7760 [Abstract] [Full Text]  
• Siu, K.-L., Kok, K.-H., Ng, M.-H. J., Poon, V. K. M., Yuen, K.-Y., Zheng, B.-J., Jin, D.-Y. (2009). Severe Acute Respiratory Syndrome Coronavirus M Protein Inhibits Type I Interferon Production by Impeding the Formation of TRAF3{middle dot}TANK{middle dot}TBK1/IKK{epsilon} Complex. J. Biol. Chem. 284: 16202-16209 [Abstract] [Full Text]  
• Umbach, J. L., Cullen, B. R. (2009). The role of RNAi and microRNAs in animal virus replication and antiviral immunity. Genes Dev. 23: 1151-1164 [Abstract] [Full Text]  

Home | Help | Feedback | Subscriptions | Archive | Search