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PMID:11438662
| Citation |
Eischen, CM, Woo, D, Roussel, MF and Cleveland, JL (2001) Apoptosis triggered by Myc-induced suppression of Bcl-X(L) or Bcl-2 is bypassed during lymphomagenesis. Mol. Cell. Biol. 21:5063-70 |
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| 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. |
| Links |
PubMed PMC87232 Online version:10.1128/MCB.21.15.5063-5070.2001 |
| Keywords |
ADP-Ribosylation Factor 1/metabolism; Animals; Apoptosis; Blotting, Northern; Blotting, Western; Cell Survival; Cells, Cultured; Lymph Nodes/metabolism; Mice; Mice, Knockout; Mice, Transgenic; Myeloid Cells/metabolism; Proto-Oncogene Proteins c-bcl-2/metabolism; Proto-Oncogene Proteins c-myc/metabolism; RNA/metabolism; Stem Cells/metabolism; Time Factors; Transformation, Genetic; Tumor Suppressor Protein p53/metabolism; bcl-X Protein |
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Significance
Annotations
| Gene product | Qualifier | GO ID | GO term name | Evidence Code | with/from | Aspect | Notes | Status |
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