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FOXO3a Provides a Quickstep from Autophagy Inhibition to Apoptosis in Cancer Therapy

Patrice Codogno1, Etienne Morel1

  • 1INSERM U1151-CNRS UMR 8253, Institut Necker Enfants-Malades (INEM), 70014 Paris, France; Université Paris Descartes-Sorbonne Paris Cité, 70006 Paris, France.

Developmental Cell
|March 14, 2018
PubMed

Insights

Blocking the turnover of FOXO3a (Forkhead box O3) via autophagy enhances cancer cell apoptosis. This occurs through increased expression of the pro-apoptotic protein PUMA/BBC3, mediated by FOXO3a.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Cancer Research

Background:

  • FOXO3a, a transcription factor, regulates apoptosis and autophagy.
  • Autophagy typically facilitates FOXO3a turnover.
  • Dysregulation of these processes is implicated in cancer.

Purpose of the Study:

  • To investigate the consequences of blocking FOXO3a turnover via autophagy.
  • To elucidate the role of FOXO3a in cancer cell apoptosis.

Main Methods:

  • Cellular assays to monitor FOXO3a levels and turnover.
  • Analysis of PUMA/BBC3 expression.
  • Assessment of apoptosis induction in cancer cells.

Main Results:

  • Inhibition of autophagy led to the blockade of FOXO3a turnover.
  • Blocked FOXO3a turnover sensitized cancer cells to apoptosis.
  • FOXO3a-mediated upregulation of PUMA/BBC3 expression was observed.

Conclusions:

  • FOXO3a turnover through autophagy is a critical regulatory mechanism.
  • Blocking this turnover enhances cancer cell apoptosis by upregulating PUMA/BBC3.
  • Targeting FOXO3a turnover represents a potential therapeutic strategy for cancer.

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