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Activation of Apoptosis by Cytoplasmic Microinjection of Cytochrome c
07:42

Activation of Apoptosis by Cytoplasmic Microinjection of Cytochrome c

Published on: June 29, 2011

c-Myc-induced apoptosis in fibroblasts is inhibited by specific cytokines

E A Harrington1, M R Bennett, A Fanidi

  • 1Biochemistry of the Cell Nucleus Laboratory, Imperial Cancer Research Fund Laboratories, London, UK.

The EMBO Journal
|July 15, 1994
PubMed

Insights

Dereguled c-Myc expression triggers apoptosis in fibroblasts, but survival factors like insulin-like growth factors can prevent this cell death. This regulation is independent of cell growth signals.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Cancer Research

Background:

  • Dereguled expression of the c-Myc oncogene is implicated in various cancers.
  • Understanding the mechanisms of c-Myc-induced apoptosis is crucial for cancer therapy development.

Purpose of the Study:

  • To investigate how deregulated c-Myc expression induces apoptosis in serum-deprived fibroblasts.
  • To identify factors that inhibit Myc-induced apoptosis and elucidate the underlying mechanisms.

Main Methods:

  • Utilized serum-deprived fibroblast cell cultures.
  • Investigated the effects of specific cytokines, including insulin-like growth factors (IGFs) and platelet-derived growth factor (PDGF).
  • Assessed apoptosis inhibition across different cell cycle phases and in drug-induced cell cycle arrest.

Main Results:

  • Cytokines, particularly IGFs and PDGF, inhibit c-Myc-induced apoptosis in low serum conditions.
  • Cytokine-mediated protection is independent of their growth-promoting abilities.
  • Apoptosis inhibition occurs in post-commitment cell cycle phases (S/G2/M) and in cells with drug-induced cell cycle arrest.
  • Insulin-like growth factor 1 (IGF-I) inhibition of apoptosis proceeds without protein synthesis, indicating no requirement for immediate early gene expression.

Conclusions:

  • c-Myc-induced apoptosis is a physiological process regulated by the availability of survival factors, not a result of conflicting growth signals.
  • Survival factors play a critical role in modulating c-Myc's apoptotic function.
  • These findings have implications for understanding mammalian cell growth regulation in vivo and potential therapeutic strategies targeting c-Myc-driven cancers.

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