c-Myc functionally cooperates with Bax to induce apoptosis

Mol Cell Biol. 2002 Sep;22(17):6158-69. doi: 10.1128/MCB.22.17.6158-6169.2002.

Abstract

c-Myc promotes apoptosis by destabilizing mitochondrial integrity, leading to the release of proapoptotic effectors including holocytochrome c. Candidate mediators of c-Myc in this process are the proapoptotic members of the Bcl-2 family. We show here that fibroblasts lacking Bak remain susceptible to c-Myc-induced apoptosis whereas bax-deficient fibroblasts are resistant. However, despite this requirement for Bax, c-Myc activation exerts no detectable effects on Bax expression, localization, or conformation. Moreover, susceptibility to c-Myc-induced apoptosis can be restored in bax-deficient cells by ectopic expression of Bax or by microinjection of a peptide comprising a minimal BH3 domain. Microinjection of BH3 peptide also restores sensitivity to c-Myc-induced apoptosis in p53-deficient primary fibroblasts that are otherwise resistant. By contrast, there is no synergy between BH3 peptide and c-Myc in fibroblasts deficient in both Bax and Bak. We conclude that c-Myc triggers a proapoptotic mitochondrial destabilizing activity that cooperates with proapoptotic members of the Bcl-2 family.

MeSH terms

  • Amino Acid Sequence
  • Animals
  • Apoptosis / genetics
  • Apoptosis / physiology*
  • Cell Line
  • Cytochrome c Group / analysis
  • Embryo, Mammalian
  • Fibroblasts / cytology
  • Genes, myc
  • Genes, p53
  • Genetic Complementation Test
  • Membrane Proteins / deficiency
  • Membrane Proteins / genetics
  • Membrane Proteins / physiology
  • Mice
  • Mice, Knockout
  • Microinjections
  • Mitochondria / enzymology
  • Molecular Sequence Data
  • Peptide Fragments / pharmacology
  • Promoter Regions, Genetic
  • Protein Conformation
  • Protein Structure, Tertiary
  • Proto-Oncogene Proteins / chemistry
  • Proto-Oncogene Proteins / deficiency
  • Proto-Oncogene Proteins / genetics
  • Proto-Oncogene Proteins / physiology*
  • Proto-Oncogene Proteins c-bcl-2 / antagonists & inhibitors
  • Proto-Oncogene Proteins c-myc / physiology*
  • Rats
  • Recombinant Fusion Proteins / physiology
  • Structure-Activity Relationship
  • Transfection
  • Tumor Suppressor Protein p53 / deficiency
  • Tumor Suppressor Protein p53 / physiology
  • bcl-2 Homologous Antagonist-Killer Protein
  • bcl-2-Associated X Protein
  • bcl-X Protein

Substances

  • Bak1 protein, mouse
  • Bak1 protein, rat
  • Bax protein, mouse
  • Bax protein, rat
  • Bcl2l1 protein, mouse
  • Bcl2l1 protein, rat
  • Cytochrome c Group
  • Membrane Proteins
  • Peptide Fragments
  • Proto-Oncogene Proteins
  • Proto-Oncogene Proteins c-bcl-2
  • Proto-Oncogene Proteins c-myc
  • Recombinant Fusion Proteins
  • Tumor Suppressor Protein p53
  • bcl-2 Homologous Antagonist-Killer Protein
  • bcl-2-Associated X Protein
  • bcl-X Protein