ArticleJournal of hepatology2021
Focal adhesion kinase (FAK) promotes cholangiocarcinoma development and progression via YAP activation.
Article in Journal of hepatology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers, 1 of them a synthesis that pooled it.
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Who cites it
70 citing papers in PubMed, 1 synthesis or guideline pooled it, 100 citations in OpenAlex.
- Focal Adhesion Kinase (FAK)-Hippo/YAP transduction signaling mediates the stimulatory effects exerted by S100A8/A9-RAGE system in triple-negative breast cancer (TNBC).Journal of experimental & clinical cancer research : CR · 2022Pooled it
- Article
- N6-methyladenosine-mediated upregulation of PAICS promotes lung-adenocarcinoma metastasis via the integrin-FAK signaling.Oncogene · 2026Article
- Functional genomic screens uncover FERMT2 as a critical regulator of YAP/TAZ-driven tumorigenicity.Cell death and differentiation · 2026Article
- BUB1 regulates cell proliferation and apoptosis in cervical cancer by AKT signaling and autophagosome-lysosome fusion via ACTN1.iScience · 2026Article
- From steatosis to metastasis: microenvironmental reprogramming of the liver in metabolic dysfunction-associated steatotic liver disease.Clinical and molecular hepatology · 2026Review
- Non-receptor tyrosine kinase signaling pathways and therapeutic implications.Signal transduction and targeted therapy · 2026Review
- RANBP1 promotes oral cancer progression through activating YAP1 and NDUFB3 derived from the database of single-cell sequencing.Cancer cell international · 2026Article
- Piperlongumine inhibits the proliferation and migration of non-small cell lung cancer cells through the EGFR/FAK/STAT3 pathway.Molecular biology reports · 2026Article
- Nuclear Mechanotransduction Across the Metastatic Cascade: Decoding Spatiotemporal Heterogeneity in Cancer Dissemination.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- Targeting TYRO3 attenuates apoptotic cell-driven cancer stemness in triple negative breast cancer.Cell communication and signaling : CCS · 2026Article
- Single-stranded DNA in the bone microenvironment promotes prostate cancer bone metastasis via the ITGA6-FAK pathway.Communications biology · 2026Article
- Preclinical mouse models for studying cholangiocarcinoma.Liver research (Beijing, China) · 2026Review
- Activation of SV2B Inhibits Matrix-Stiffness-Induced Tumorigenesis and EMT in Glioma via FAK/PI3K/AKT Signaling Pathway.Oncology and therapy · 2026Article
- Cancer-associated fibroblast-derived stanniocalcin 1 promotes cholangiocarcinoma progression and lymph node metastasis.Fundamental research · 2026Article
- Focal adhesion kinase inhibition enhances response to checkpoint immunotherapy in hepatocellular carcinoma.Journal of translational internal medicine · 2026Article
- Focal Adhesion and Cancer Cell Cycle-Associated Resistance.ACS omega · 2026Review
- VIRMA/IGF2BP3-mediated ANLN upregulation promotes intrahepatic cholangiocarcinoma growth by forming a positive feedback loop with RhoA/YAP1/TEAD1 signaling pathway.Cell death & disease · 2026Article
- CDK4/6-targeted therapy for gastrointestinal cancers: from resistance mechanisms to immuno-combination strategies guided by biomarkers.Frontiers in immunology · 2026Review
- IGF1/IGF-1R promotes hepatocellular carcinoma progression by activating the Akt/GSK-3β pathway.PloS one · 2026Article
10 more citing papers are in PubMed but not listed here.
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Authors and funding
18 authors at 9 institutions in 4 countries.
Funding
Abstract
BACKGROUND &
aimsFocal adhesion kinase (FAK) is a non-receptor tyrosine kinase that is upregulated in many tumor types and is a promising target for cancer therapy. Herein, we elucidated the functional role of FAK in intrahepatic cholangiocarcinoma (iCCA) development and progression.
methodsExpression levels and activation status of FAK were determined in human iCCA samples. The functional contribution of FAK to Akt/YAP murine iCCA initiation and progression was investigated using conditional Fak knockout mice and constitutive Cre or inducible Cre mice, respectively. The oncogenic potential of FAK was further examined via overexpression of FAK in mice. In vitro cell line studies and in vivo drug treatment were applied to address the therapeutic potential of targeting FAK for iCCA treatment.
resultsFAK was ubiquitously upregulated and activated in iCCA lesions. Ablation of FAK strongly delayed Akt/YAP-driven mouse iCCA initiation. FAK overexpression synergized with activated AKT to promote iCCA development and accelerated Akt/Jag1-driven cholangiocarcinogenesis. Mechanistically, FAK was required for YAP(Y357) phosphorylation, supporting the role of FAK as a central YAP regulator in iCCA. Significantly, ablation of FAK after Akt/YAP-dependent iCCA formation strongly suppressed tumor progression in mice. Furthermore, a remarkable iCCA growth reduction was achieved when a FAK inhibitor and palbociclib, a CDK4/6 inhibitor, were administered simultaneously in human iCCA cell lines and Akt/YAP mice.
conclusionsFAK activation contributes to the initiation and progression of iCCA by inducing the YAP proto-oncogene. Targeting FAK, either alone or in combination with anti-CDK4/6 inhibitors, may be an effective strategy for iCCA treatment. LAY SUMMARY: We found that the protein FAK (focal adhesion kinase) is upregulated and activated in human and mouse intrahepatic cholangiocarcinoma samples. FAK promotes intrahepatic cholangiocarcinoma development, whereas deletion of FAK strongly suppresses its initiation and progression. Combined FAK and CDK4/6 inhibitor treatment had a strong anti-cancer effect in in vitro and in vivo models. This combination therapy might represent a valuable and novel treatment against human intrahepatic cholangiocarcinoma.
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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.