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SUMOylation inhibits FOXM1 activity and delays mitotic transition

S S Myatt1, M Kongsema1, C W-Y Man2

  • 1Department of Surgery and Cancer, Imperial College London, Imperial Centre for Translational and Experimental Medicine (ICTEM), London, UK.

Oncogene
|December 24, 2013
PubMed

Insights

SUMOylation of FOXM1 (forkhead box transcription factor) inhibits its activity, promoting cell cycle arrest and degradation. This process is crucial for the cellular response to DNA damage and chemotherapy.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Cancer Research

Background:

  • FOXM1 (forkhead box transcription factor) is vital for cell cycle progression and DNA damage response.
  • Dysregulation of FOXM1 is common in various cancers.
  • Post-translational modifications, like SUMOylation, can regulate protein function.

Purpose of the Study:

  • To investigate the role of SUMOylation in regulating FOXM1 activity and its impact on cell cycle control.
  • To explore how SUMOylation affects FOXM1 localization, stability, and function in response to cellular stress.

Main Methods:

  • SUMOylation assays using wild-type and mutant FOXM1 (SUMOylation-deficient and auto-SUMOylating FOXM1-Ubc9).
  • Analysis of FOXM1 localization, ubiquitination, and degradation.
  • Cell proliferation assays and cell cycle analysis (mitotic entry/exit).
  • Treatment of MCF-7 breast cancer cells with epirubicin and mitotic inhibitors.

Main Results:

  • FOXM1 undergoes dynamic SUMOylation, particularly in response to epirubicin and mitotic inhibitors.
  • SUMOylation of FOXM1 inhibits its transcriptional activity, promotes cytoplasmic localization, and enhances its degradation via APC/Cdh1.
  • A SUMOylation-deficient FOXM1 mutant increased cell proliferation.
  • The FOXM1-Ubc9 fusion protein led to persistent cyclin B1 expression and delayed mitotic exit.

Conclusions:

  • SUMOylation acts as a negative regulator of FOXM1 activity.
  • SUMOylation-mediated regulation of FOXM1 is critical for mitotic delay and cellular response to cytotoxic drugs.
  • Targeting FOXM1 SUMOylation could be a therapeutic strategy in cancer treatment.

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