ArticleGut2023
FAK suppresses antigen processing and presentation to promote immune evasion in pancreatic cancer.
Article in Gut, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
42 citing papers in PubMed, 70 citations in OpenAlex.
- Endothelial Cell pY397-FAK Expression Predicts the Risk of Breast Cancer Recurrences after Radiotherapy in the SweBCG91-RT Cohort.Clinical cancer research : an official journal of the American Association for Cancer Research · 2025Trial
- PINK1 promotes the progression of lung squamous cell carcinoma through the FAK/AKT/RhoA/vinculin pathway.Oncology reports · 2026Article
- Review
- N6-methyladenosine-mediated upregulation of PAICS promotes lung-adenocarcinoma metastasis via the integrin-FAK signaling.Oncogene · 2026Article
- Advances, challenges, and innovative strategies of CAR-T cell therapy in pancreatic cancer.Biomarker research · 2026Review
- Article
- Tumor-Derived LAMB3 Drives Immunosuppressive LRRC15Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- The CD49b (ITGA2) collagen receptor excludes CD8iScience · 2026Article
- The retinol-metabolizing enzyme DHRS3 coordinates antigen presentation, endothelial stability, and cholesterol metabolism to suppress hepatocellular carcinoma progression.The Journal of biological chemistry · 2026Article
- Tumor cell intrinsic mechanisms of immune escape.Cell communication and signaling : CCS · 2026Review
- Disarming cancer resistance: FAK as a therapeutic target.Trends in cancer · 2026Review
- The Aging Microenvironment Is a Determinant of Immune Exclusion and Metastatic Fate in Pancreatic Cancer.Cancer research · 2026Article
- Decoding the diabetes-pancreatic adenocarcinoma connection: the critical role of PILRA in intermediate monocyte activity.BMC medical genomics · 2026Article
- Peritoneal metastasis in pancreatic cancer: molecular mechanisms, microenvironmental remodeling, and emerging intraperitoneal interventions.Frontiers in molecular biosciences · 2026Review
- Rethinking PDAC: from immunological silence to therapeutic opportunity.Frontiers in immunology · 2026Review
- Identification of key genes in pancreatic ductal adenocarcinoma with biologically informed deep neural network.Journal of gastrointestinal oncology · 2025Article
- Pan-cancer multi-omics profiling reveals ubiquitin D as a novel biomarker for diagnosis, immune microenvironment remodeling and prognostic prediction.Discover oncology · 2025Article
- Immune evasion in cancer: mechanisms and cutting-edge therapeutic approaches.Signal transduction and targeted therapy · 2025Review
- Review
- CMSS1: A RNA binding protein with pivotal roles in non-small cell lung cancer progression and prognosis.BMC cancer · 2025Article
Corrections and comments
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Authors and funding
11 authors at 5 institutions in 2 countries.
Funding
Abstract
objectiveImmunotherapy for the treatment of pancreatic ductal adenocarcinoma (PDAC) has shown limited efficacy. Poor CD8 T-cell infiltration, low neoantigen load and a highly immunosuppressive tumour microenvironment contribute to this lack of response. Here, we aimed to further investigate the immunoregulatory function of focal adhesion kinase (FAK) in PDAC, with specific emphasis on regulation of the type-II interferon response that is critical in promoting T-cell tumour recognition and effective immunosurveillance.
designWe combined CRISPR, proteogenomics and transcriptomics with mechanistic experiments using a Kras
resultsLoss of PDAC cell-intrinsic FAK signalling promotes expression of the immunoproteasome and Major Histocompatibility Complex class-I (MHC-I), resulting in increased antigen diversity and antigen presentation by FAK-/- PDAC cells. Regulation of the immunoproteasome by FAK is a critical determinant of this response, optimising the physicochemical properties of the peptide repertoire for high affinity binding to MHC-I. Expression of these pathways can be further amplified in a STAT1-dependent manner via co-depletion of FAK and STAT3, resulting in extensive infiltration of tumour-reactive CD8 T-cells and further restraint of tumour growth. FAK-dependent regulation of antigen processing and presentation is conserved between mouse and human PDAC, but is lost in cells/tumours with an extreme squamous phenotype.
conclusionTherapies aimed at FAK degradation may unlock additional therapeutic benefit for the treatment of PDAC through increasing antigen diversity and promoting antigen presentation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.