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Nuclear FAK and Runx1 Cooperate to Regulate IGFBP3, Cell-Cycle Progression, and Tumor Growth

Marta Canel1,2, Adam Byron1, Andrew H Sims1

  • 1Cancer Research UK Edinburgh Centre, Institute of Genetics and Molecular Medicine, University of Edinburgh, Edinburgh, United Kingdom.

Cancer Research
|August 16, 2017
PubMed

Insights

Nuclear focal adhesion kinase (FAK) regulates gene expression in skin cancer. This study reveals FAK’s role in a novel molecular complex controlling tumor growth and cell-cycle progression.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Nuclear focal adhesion kinase (FAK) is implicated in cancer gene expression.
  • FAK influences cellular function and the tumor microenvironment.

Purpose of the Study:

  • Investigate the role of nuclear FAK in skin squamous cell carcinoma (SCC).
  • Elucidate the mechanism by which FAK regulates SCC cell-cycle progression and tumor growth.

Main Methods:

  • Utilized a murine model of skin SCC.
  • Identified and characterized a novel molecular complex involving FAK and Runx1 in SCC cell nuclei.
  • Analyzed FAK interactions with Runx1-regulatory proteins and epigenetic modifiers.

Main Results:

  • Nuclear FAK was found to regulate Runx1-dependent transcription of insulin-like growth factor binding protein 3 (IGFBP3).
  • This regulation impacts SCC cell-cycle progression and tumor growth in vivo.
  • A novel FAK-Runx1 molecular complex was identified, interacting with epigenetic modifiers like Sin3a.

Conclusions:

  • FAK acts as a scaffolding protein within nuclear molecular complexes that control gene transcription.
  • These findings offer new insights into FAK's function in regulating gene expression and tumor progression in SCC.

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