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pubmed-article:11024153pubmed:issue21lld:pubmed
pubmed-article:11024153pubmed:dateCreated2000-11-20lld:pubmed
pubmed-article:11024153pubmed:abstractTextThe tumorigenic potential of the Burkitt lymphoma (BL) cell line Akata is dependent on the restricted latency program of Epstein-Barr virus (EBV) that is characteristically maintained in BL tumors. Within these cells, EBV-mediated inhibition of apoptosis correlates with an up-regulation of BCL-2 levels in concert with a down-regulation in c-MYC expression that occurs under growth-limiting conditions. Here we addressed whether EBV's effects on apoptosis and tumorigenicity are mediated by the EBV small RNAs EBER-1 and EBER-2. Stable expression of the EBERs in EBV-negative Akata BL cells, at levels comparable to those in EBV-positive cells, significantly enhanced the tumorigenic potential of EBV-negative BL cells in SCID mice, but did not fully restore tumorigenicity relative to EBV-positive Akata cells. Furthermore, wild-type or greater levels of EBER expression in EBV-negative Akata cells did not promote BL cell survival. These data therefore suggest that EBV can contribute to BL through at least two avenues: an EBER-dependent mechanism that enhances tumorigenic potential independent of a direct effect on apoptosis, and a second mechanism, mediated by an as-yet-unidentified EBV gene(s), that offsets the proapoptotic consequences of deregulated c-MYC in BL.lld:pubmed
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pubmed-article:11024153pubmed:authorpubmed-author:YangCClld:pubmed
pubmed-article:11024153pubmed:authorpubmed-author:ClevelandJ...lld:pubmed
pubmed-article:11024153pubmed:authorpubmed-author:SampleJ TJTlld:pubmed
pubmed-article:11024153pubmed:authorpubmed-author:SunH SHSlld:pubmed
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pubmed-article:11024153pubmed:dateRevised2009-11-18lld:pubmed
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