ArticleThe Journal of biological chemistry2016
A Hippo and Fibroblast Growth Factor Receptor Autocrine Pathway in Cholangiocarcinoma.
Article in The Journal of biological chemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers, 1 of them a synthesis that pooled it.
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Who cites it
56 citing papers in PubMed, 1 synthesis or guideline pooled it, 97 citations in OpenAlex.
- Molecular Targets and Signaling Pathways in Cholangiocarcinoma: A Systematic Review.Asian Pacific journal of cancer prevention : APJCP · 2023Pooled it
- A High-Fidelity and Ancestrally Inclusive Patient-Derived Organoid Platform Resolves Cancer Cell Plasticity in Uterine Carcinosarcoma.bioRxiv : the preprint server for biology · 2026Article
- Molecular mechanisms and genetic features of cholangiocarcinoma: implications for targeted therapeutic strategies.Precision clinical medicine · 2025Review
- Integrative High-Throughput RNAi Screening Identifies BRSK1, STK32C and STK40 as Novel Activators of YAP/TAZ.International journal of molecular sciences · 2025Article
- The Role of Hippo Signaling in Brain Arteriovenous Malformations: Molecular Insights into Post-Embolization Remodeling.International journal of molecular sciences · 2025Article
- YAP/TAZ Signalling Controls Epidermal Keratinocyte Fate.International journal of molecular sciences · 2024Review
- Article
- The RNA methyltransferase METTL16 enhances cholangiocarcinoma growth through PRDM15-mediated FGFR4 expression.Journal of experimental & clinical cancer research : CR · 2023Article
- Review
- LCK inhibition downregulates YAP activity and is therapeutic in patient-derived models of cholangiocarcinoma.Journal of hepatology · 2023Article
- Calcyclin-binding protein contributes to cholangiocarcinoma progression by inhibiting ubiquitination of MCM2.Oncology research · 2023Article
- Selecting an Appropriate Experimental Animal Model for Cholangiocarcinoma Research.Journal of clinical and translational hepatology · 2022Review
- Hippo signalling in the liver: role in development, regeneration and disease.Nature reviews. Gastroenterology & hepatology · 2022Review
- Regorafenib inhibits epithelial-mesenchymal transition and suppresses cholangiocarcinoma metastasis via YAP1-AREG axis.Cell death & disease · 2022Article
- Urolithin A targets the AKT/WNK1 axis to induce autophagy and exert anti-tumor effects in cholangiocarcinoma.Frontiers in oncology · 2022Article
- Advances in prognostic and therapeutic targets for hepatocellular carcinoma and intrahepatic cholangiocarcinoma: The hippo signaling pathway.Frontiers in oncology · 2022Review
- Inflammatory pathways and cholangiocarcinoma risk mechanisms and prevention.Advances in cancer research · 2022Review
- YAP1 activation and Hippo pathway signaling in the pathogenesis and treatment of intrahepatic cholangiocarcinoma.Advances in cancer research · 2022Review
- Cholangiocarcinoma: the role of genetic and epigenetic factors; current and prospective treatment with checkpoint inhibitors and immunotherapy.American journal of translational research · 2021Review
- The Application Progress of Patient-Derived Tumor Xenograft Models After Cholangiocarcinoma Surgeries.Frontiers in oncology · 2021Review
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
Abstract
Herein, we have identified cross-talk between the Hippo and fibroblast growth factor receptor (FGFR) oncogenic signaling pathways in cholangiocarcinoma (CCA). Yes-associated protein (YAP) nuclear localization and up-regulation of canonical target genes was observed in CCA cell lines and a patient-derived xenograft (PDX). Expression of FGFR1, -2, and -4 was identified in human CCA cell lines, driven, in part, by YAP coactivation of TBX5. In turn, FGFR signaling in a cell line with minimal basal YAP expression induced its cellular protein expression and nuclear localization. Treatment of YAP-positive CCA cell lines with BGJ398, a pan-FGFR inhibitor, resulted in a decrease in YAP activation. FGFR activation of YAP appears to be driven largely by FGF5 activation of FGFR2, as siRNA silencing of this ligand or receptor, respectively, inhibited YAP nuclear localization. BGJ398 treatment of YAP-expressing cells induced cell death due to Mcl-1 depletion. In a YAP-associated mouse model of CCA, expression of FGFR 1, 2, and 4 was also significantly increased. Accordingly, BGJ398 treatment was tumor-suppressive in this model and in a YAP-positive PDX model. These preclinical data suggest not only that the YAP and Hippo signaling pathways culminate in an Mcl-1-regulated tumor survival pathway but also that nuclear YAP expression may be a biomarker to employ in FGFR-directed therapy.
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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.