Nuclear FAK Controls Chemokine Transcription, Tregs, and Evasion of Anti-tumor Immunity
Open accessAbstract
Focal adhesion kinase (FAK) promotes anti-tumor immune evasion. Specifically, the kinase activity of nuclear-targeted FAK in squamous cell carcinoma (SCC) cells drives exhaustion of CD8(+) T cells and recruitment of regulatory T cells (Tregs) in the tumor microenvironment by regulating chemokine/cytokine and ligand-receptor networks, including via transcription of Ccl5, which is crucial. These changes inhibit antigen-primed cytotoxic CD8(+) T cell activity, permitting growth of FAK-expressing tumors. Mechanistically, nuclear FAK is associated with chromatin and exists in complex with transcription factors and their upstream regulators that control Ccl5 expression. Furthermore, FAK's immuno-modulatory nuclear activities may be specific to cancerous squamous epithelial cells, as normal keratinocytes do not have nuclear FAK. Finally, we show that a small-molecule FAK kinase inhibitor, VS-4718, which is currently in clinical development, also drives depletion of Tregs and promotes a CD8(+) T cell-mediated anti-tumor response. Therefore, FAK inhibitors may trigger immune-mediated tumor regression, providing previously unrecognized therapeutic opportunities.
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FAK-related fibrosis can form a barrier in tumors that limits the CD8+ T cells infiltration in tumors, and FAK inhibition can ultimately promote the antitumor effects by decreasing the number of tumor-resident Tregs.
“FAK-related fibrosis can form a barrier in tumors that limits the CD8+ T cells infiltration in tumors, and FAK inhibition can ultimately promote the antitumor effects by decreasing the number of tumor-resident Tregs.”
From Targeting KRAS mutant cancers: from druggable therapy to drug resistance (2022) · cites this paper as [126]
FAK inhibition may enhance KRAS (G12C) inhibition and immunotherapy.
“Thus, FAK inhibition may enhance KRAS (G12C) inhibition and immunotherapy [125, 126].”
From Targeting KRAS mutant cancers: from druggable therapy to drug resistance (2022) · cites this paper as [126]
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- Authors
- Serrels, A., Lund, T., Serrels, B., Byron, A., McPherson, R. C., von Kriegsheim, A., Gómez-Cuadrado, L., Canel, M., Muir, M., Ring, J. E., Maniati, E., Sims, A. H., Pachter, J. A., Brunton, V. G., Gilbert, N., Anderton, S. M., Nibbs, R. J. B., & Frame, M. C.
- Affiliations
- Edinburgh Cancer Research (GB)
- Centre for Inflammation Research (GB)
- Verastem (United States) (US)
- Queen Mary University of London (GB)
- Institute of Genetics and Cancer (GB)
- University of Glasgow (GB)
- Corresponding author
- Serrels, Alan
- Frame, Margaret C.
- ORCID
- Venue
- Cell
- Publisher
- Elsevier BV
- Published
- 2015-09
- Volume
- 163
- Issue
- 1
- Pages
- 160-173
- ISSN
- 0092-8674 (ISSN-L)
- PMC
- PMC4597190
- OpenAlex
- W2102498455
- Cited by
- 407
- References
- 62
- Citations by year
- 2026: 29 · 2025: 33 · 2024: 42 · 2023: 39 · 2022: 47 · 2021: 52 · 2020: 37 · 2019: 45 · 2018: 32 · 2017: 24 · 2016: 26 · 2015: 1
- FWCI
- 12.38
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Locations
- Cell (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Research Explorer (The University of Manchester) (publishedVersion, cc-by)
- ENLIGHTEN (Jurnal Bimbingan dan Konseling Islam) (acceptedVersion)
- Repositorio Institucional de la Universidad de Burgos (University of Burgos) (submittedVersion, cc-by)
- UCL Discovery (University College London) (submittedVersion)
- Edinburgh Research Explorer (University of Edinburgh) (submittedVersion, cc-by)
- Funders
- Wellcome Trust (095831)
- Verastem Oncology
- Cancer Research UK (C157/A15703, 15703)
- Science Foundation Ireland (13/SIRG/2174, 06/CE/B1129)
- Medical Research Council (G1100084)
- Topics
- Health Sciences › Medicine › Oncology › Cancer Immunotherapy and Biomarkers
- Health Sciences › Medicine › Immunology and Allergy › Cell Adhesion Molecules Research
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Keywords
- focal adhesion kinase, chemokine transcription, RANTES, regulatory T cells, CD8+ T cell exhaustion, tumor immune evasion, squamous cell carcinoma, tumor microenvironment, VS-4718, antitumor immunity, chromatin, keratinocytes
- MeSH terms
- Aminopyridines, Animals, Carcinoma, Squamous Cell, Disease Models, Animal, Humans, Mice, Nude, Skin Neoplasms, Transcription, Genetic, Keratinocytes, Chemokine CCL5, Tumor Escape, T-Lymphocytes, Regulatory, Mice, Focal Adhesion Protein-Tyrosine Kinases
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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