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Epstein-barr virus small rnas potentiate tumorigenicity of burkitt lymphoma cells independently of an effect on apoptosis

Academic Article
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Overview

authors

  • Ruf, I. K.
  • Rhyne, P. W.
  • Yang, C. Y.
  • Cleveland, John
  • Sample, J. T.

publication date

  • November 2000

journal

  • Journal of Virology  Journal

abstract

  • The 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.

subject areas

  • Animals
  • Apoptosis
  • Burkitt Lymphoma
  • Cell Line, Transformed
  • Herpesvirus 4, Human
  • Humans
  • Mice
  • Mice, SCID
  • RNA, Viral
  • Tumor Cells, Cultured
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Identity

International Standard Serial Number (ISSN)

  • 0022-538X

Digital Object Identifier (DOI)

  • 10.1128/jvi.74.21.10223-10228.2000

PubMed ID

  • 11024153
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Additional Document Info

start page

  • 10223

end page

  • 10228

volume

  • 74

issue

  • 21

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