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FOXO transcription factors in cell-cycle regulation and the response to oxidative stress

Yoko Furukawa-Hibi1, Yosuke Kobayashi, Chen Chen

  • 1Department of Geriatric Research, National Institute for Longevity Sciences, National Center for Geriatrics and Gerontology, Morioka, Obu, Aichi, Japan.

Antioxidants & Redox Signaling
|May 14, 2005
PubMed

Insights

Forkhead box O (FOXO) transcription factors regulate key cellular processes and are negatively controlled by the PI3K-Akt pathway. Stress activates FOXO proteins, suggesting a tumor suppressor role similar to p53.

Area of Science:

  • Molecular Biology
  • Cellular Biology
  • Biochemistry

Background:

  • Mammalian forkhead box O (FOXO) transcription factors (FOXO1, FOXO3a, FOXO4) are crucial regulators of cellular processes.
  • These processes include cell cycle, apoptosis, DNA repair, stress resistance, and metabolism.
  • FOXO activity is modulated by the phosphatidylinositol 3-kinase-Akt (PI3K-Akt) signaling pathway, often activated by growth factors and cytokines.

Purpose of the Study:

  • To elucidate the regulatory mechanisms of FOXO transcription factors.
  • To investigate the role of oxidative stress in FOXO protein activity.
  • To explore the potential tumor suppressor function of FOXO proteins.

Main Methods:

  • Analysis of FOXO protein regulation by signaling pathways.
  • Investigation of FOXO protein response to oxidative stress.
  • Comparison of FOXO activity with known tumor suppressors like p53.

Main Results:

  • FOXO proteins are negatively regulated by the PI3K-Akt signaling pathway.
  • Oxidative stress induces FOXO protein phosphorylation, nuclear translocation, and acetylation-deacetylation.
  • Stress-induced FOXO activation leads to cell-cycle arrest gene expression.

Conclusions:

  • FOXO transcription factors play a significant role in cellular stress responses.
  • FOXO proteins are activated by stress, similar to the tumor suppressor p53.
  • Evidence suggests FOXO proteins function as tumor suppressors by inducing cell-cycle arrest.

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