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Apoptosis triggered by myc-induced suppression of bcl-x-l or bcl-2 is bypassed during lymphomagenesis

Academic Article
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Overview

authors

  • Eischen, C. M.
  • Woo, D.
  • Roussel, M. F.
  • Cleveland, John

publication date

  • August 2001

journal

  • Molecular and Cellular Biology  Journal

abstract

  • Enforced Bcl-2 expression inhibits Myc-induced apoptosis and cooperates with Myc in transformation. Here we report that the synergy between Bcl-2 and Myc in transforming hematopoietic cells in fact reflects a Myc-induced pathway that selectively suppresses the expression of the Bcl-X(L) or Bcl-2 antiapoptotic protein. Myc activation suppresses Bcl-X(L) RNA and protein levels in cultures of primary myeloid and lymphoid progenitors, and Bcl-X(L) and Bcl-2 expression is inhibited by Myc in precancerous B cells from Emu-myc transgenic mice. The suppression of bcl-X RNA levels by Myc requires de novo protein synthesis, indicating that repression is indirect. Importantly, the suppression of Bcl-2 or Bcl-X(L) by Myc is corrupted during Myc-induced tumorigenesis, as Bcl-2 and/or Bcl-X(L) levels are markedly elevated in over one-half of all lymphomas arising in Emicro-myc transgenic mice. Bcl-2 and/or Bcl-X(L) overexpression did not correlate with loss of ARF or p53 function in tumor cells, indicating that these two apoptotic pathways are inactivated independently. Therefore, the suppression of Bcl-X(L) or Bcl-2 expression represents a physiological Myc-induced apoptotic pathway that is frequently bypassed during lymphomagenesis.

subject areas

  • ADP-Ribosylation Factor 1
  • Animals
  • Apoptosis
  • Blotting, Northern
  • Blotting, Western
  • Cell Survival
  • Cells, Cultured
  • Lymph Nodes
  • Mice
  • Mice, Knockout
  • Mice, Transgenic
  • Myeloid Cells
  • Proto-Oncogene Proteins c-bcl-2
  • Proto-Oncogene Proteins c-myc
  • RNA
  • Stem Cells
  • Time Factors
  • Transformation, Genetic
  • Tumor Suppressor Protein p53
  • bcl-X Protein
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Identity

International Standard Serial Number (ISSN)

  • 0270-7306

Digital Object Identifier (DOI)

  • 10.1128/mcb.21.15.5063-5070.2001

PubMed ID

  • 11438662
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Additional Document Info

start page

  • 5063

end page

  • 5070

volume

  • 21

issue

  • 15

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