Journal
ONCOGENE
Volume 33, Issue 10, Pages 1258-1264Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/onc.2013.71
Keywords
EBV; BART miRNAs; apoptosis; RISC-IP; Burkitt's lymphoma
Funding
- National Cancer Institute, National Institutes of Health [P01 CA022443, R01 CA133027, R01 CA070723]
- Deutsche Forschungsgemeinschaft [SFB455, SEBTR5]
- National Cancer Center
- DAAD, German Academic Exchange Service
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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 EBVs 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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