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Journal of Virology, April 2009, p. 3333-3341, Vol. 83, No. 7
0022-538X/09/$08.00+0 doi:10.1128/JVI.01689-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.
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Center for Integrated Protein Sciences Munich (CIPSM), Laboratory of RNA Biology, Max Planck Institute of Biochemistry, Am Klopferspitz 18, 82152 Martinsried, Germany,1 Institute of Microbiology and Hygiene, Department of Virology, University of Homburg/Saar, House 47, 66421 Homburg/Saar, Germany,2 Department of Pathology, The University of Hong Kong, Pok Fu Lam, Hong Kong3
Received 8 August 2008/ Accepted 1 January 2009
MicroRNAs (miRNAs) represent a conserved class of small noncoding RNAs that are found in all higher eukaryotes as well as some DNA viruses. miRNAs are 20 to 25 nucleotides in length and have important regulatory functions in biological processes such as embryonic development, cell differentiation, hormone secretion, and metabolism. Furthermore, miRNAs have been implicated in the pathology of various diseases, including cancer. miRNA expression profiles not only classify different types of cancer but also may even help to characterize distinct tumor stages, therefore constituting a valuable tool for prognosis. Here we report the miRNA profile of Epstein-Barr virus (EBV)-positive nasopharyngeal carcinoma (NPC) tissue samples characterized by cloning and sequencing. We found that all EBV miRNAs from the BART region are expressed in NPC tissues, whereas EBV miRNAs from the BHRF1 region are not found. Moreover, we identified two novel EBV miRNA genes originating from the BART region that have not been found in other tissues or cell lines before. We also identified three new human miRNAs which might be specific for nasopharyngeal tissues. We further show that a number of different cellular miRNAs, including miR-15a and miR-16, are up- or downregulated in NPC tissues compared to control tissues. We found that the tumor suppressor BRCA-1 is a target of miR-15a as well as miR-16, suggesting a miRNA role in NPC pathogenesis.
Published ahead of print on 14 January 2009.
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