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FAK goes nuclear to control antitumor immunity-a new target in cancer immuno-therapy

Alan Serrels1, Margaret C Frame1

  • 1Cancer Research UK Edinburgh Center, Institute of Genetics and Molecular Medicine, University of Edinburgh , Edinburgh, UK.

Oncoimmunology
|May 4, 2016
PubMed

Insights

Cancer cells evade immune attack by controlling regulatory T cells (Tregs). Nuclear Focal Adhesion Kinase (FAK) regulates Treg levels, suggesting FAK inhibitors could promote immune-mediated tumor regression.

Area of Science:

  • Oncology
  • Immunology
  • Molecular Biology

Background:

  • Tumor immune evasion is crucial for cancer progression.
  • Regulatory T cells (Tregs) play a significant role in suppressing antitumor immune responses.
  • Focal Adhesion Kinase (FAK) is a key signaling protein involved in cell functions.

Purpose of the Study:

  • To investigate the role of nuclear Focal Adhesion Kinase (FAK) activity in regulating tumor-infiltrating regulatory T cells (Tregs).
  • To explore the potential of targeting nuclear FAK activity for cancer immunotherapy.

Main Methods:

  • Analysis of nuclear FAK activity in cancer cells.
  • Assessment of Treg levels within tumors.
  • Evaluation of chemokine and cytokine gene expression in cancer cells.
  • Investigating the effects of FAK inhibitors on tumor immune microenvironment and regression.

Main Results:

  • Nuclear FAK activity was found to unexpectedly control tumor Treg levels.
  • FAK regulates the transcription of chemokines and cytokines in cancer cells, influencing immune evasion.
  • Targeting nuclear FAK activity impacts the tumor immune microenvironment.

Conclusions:

  • Nuclear FAK activity is a novel regulator of immune evasion in cancer by modulating Treg populations.
  • FAK kinase inhibitors represent a potential therapeutic strategy to overcome immune suppression and induce tumor regression.
Keywords:
Cancer immunityFocal Adhesion Kinasecheckpoint blockadechemokine transcriptiontumor microenvironment

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