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Novel functions of FoxM1: from molecular mechanisms to cancer therapy

Mónica Alvarez-Fernández1, René H Medema

  • 1Cell Division and Cancer Group, Spanish National Cancer Research Center (CNIO) Madrid, Spain.

Frontiers in Oncology
|March 8, 2013
PubMed

Insights

Forkhead box protein M1 (FoxM1) is crucial for cell cycle regulation and genomic stability. Overexpressed in cancers, FoxM1 drives tumor growth, invasion, and metastasis, presenting a potential therapeutic target.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Genetics

Background:

  • FoxM1, a transcription factor, regulates cell cycle (G2 phase) and maintains genomic stability.
  • FoxM1 overexpression is common in human cancers, correlating with tumor proliferation.
  • Recent research links FoxM1 to DNA damage response and senescence pathways.

Purpose of the Study:

  • To review and discuss the molecular mechanisms of FoxM1's roles in tumorogenesis.
  • To explore FoxM1's involvement in angiogenesis, invasion, and metastasis.
  • To evaluate FoxM1 as a potential therapeutic target in cancer treatment.

Main Methods:

  • Literature review of studies on FoxM1 function and cancer.
  • Analysis of molecular mechanisms underlying FoxM1's roles.
  • Discussion of FoxM1's implications in cancer therapy.

Main Results:

  • FoxM1 regulates cell cycle, mitosis, and genomic stability.
  • FoxM1 promotes tumor proliferation, angiogenesis, invasion, and metastasis.
  • FoxM1 is implicated in DNA damage response and senescence pathways relevant to cancer therapy.

Conclusions:

  • FoxM1 plays multifaceted roles in tumor progression and response to cancer therapies.
  • Understanding FoxM1's molecular mechanisms is key to its therapeutic potential.
  • FoxM1 represents a promising therapeutic target for various human cancers.
Keywords:
DNA damageFoxM1cancercheckpointsenescencetherapy

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