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Focal adhesion kinase is required for β-catenin-induced mobilization of epidermal stem cells

Rachel A Ridgway1, Bryan Serrels, Susan Mason

  • 1The Beatson Institute for Cancer Research, Garscube Estate, Switchback Road, Bearsden, Glasgow G61 1BD, UK.

Carcinogenesis
|September 14, 2012
PubMed

Insights

Focal adhesion kinase (FAK) is crucial for skin stem cell mobilization during carcinogenesis. Inhibiting FAK prevents tumor development by blocking beta-catenin-induced stem cell activation and c-Myc expression.

Area of Science:

  • Oncology
  • Dermatology
  • Cell Biology

Background:

  • Focal adhesion kinase (FAK) is a key mediator of integrin and growth factor signaling.
  • Previous studies demonstrated that FAK deficiency in skin prevents chemically induced skin carcinogenesis.

Purpose of the Study:

  • To investigate the role of FAK in stem cell mobilization during skin carcinogenesis.
  • To elucidate the molecular mechanisms linking FAK, beta-catenin, and stem cell activation in response to phorbol ester treatment.

Main Methods:

  • Skin-specific deletion of FAK in mice.
  • Phorbol ester treatment to induce skin carcinogenesis.
  • Analysis of stem cell mobilization from the hair follicle bulge region.
  • Western blotting and immunofluorescence to assess protein localization and activation (e.g., beta-catenin, c-Myc).

Main Results:

  • Skin-specific deletion of FAK prevented stem cell mobilization from the hair follicle bulge.
  • Phorbol ester treatment activated beta-catenin in the skin, and FAK was required for this activation and subsequent stem cell mobilization.
  • Inhibition of Src kinase activity also prevented stem cell mobilization.
  • FAK was essential for the nuclear localization of beta-catenin and transcriptional activation of c-Myc.

Conclusions:

  • FAK plays a critical role in regulating epidermal stem cell behavior during skin carcinogenesis.
  • This study reveals cross-talk between integrin and Wnt signaling pathways, mediated by FAK, in controlling stem cell dynamics and early tumorigenesis.
  • Targeting FAK may represent a therapeutic strategy for preventing skin cancer initiation.

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