Epstein-Barr virus maintains lymphomas via its miRNAs.
Oncogene 44, 1258-1264 (2014)
Epstein-Barr virus (EBV) has evolved exquisite controls over its host cells, human B lymphocytes, not only directing these cells during latency to proliferate and thereby expand the pool of infected cells, but also to survive and thereby persist for the lifetime of the infected individual. Although these activities ensure the virus is successful, they also make the virus oncogenic, particularly when infected people are immunosuppressed. Here we show, strikingly, that one set of EBV's microRNAs (miRNAs) both sustain Burkitt's lymphoma (BL) cells in the absence of other viral oncogenes and promote the transformation of primary B lymphocytes. BL cells were engineered to lose EBV and found to die by apoptosis and could be rescued by constitutively expressing viral miRNAs in them. Two of these EBV miRNAs were found to target caspase 3 to inhibit apoptosis at physiological concentrations.
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Publication type
Article: Journal article
Document type
Scientific Article
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Keywords
EBV; BART miRNAs; Apoptosis; RISC-IP; Burkitt's Lymphoma; Human Gamma-herpesviruses; Microrna Targets; Down-regulation; Lmp1 Oncogene; Protein; Ebv; Expression; Apoptosis; Cells; Bim
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Publication Year
2014
Prepublished in Year
2013
HGF-reported in Year
2013
ISSN (print) / ISBN
0950-9232
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0950-9232
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Volume: 44,
Issue: 10,
Pages: 1258-1264
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Nature Publishing Group
Publishing Place
London
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Peer reviewed
POF-Topic(s)
30203 - Molecular Targets and Therapies
Research field(s)
Immune Response and Infection
PSP Element(s)
G-501500-001
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Erfassungsdatum
2013-08-02