ArticleIn vivo (Athens, Greece)
FGF10/FGFR2 Signaling: Therapeutically Targetable Vulnerability in Ligand-responsive Cholangiocarcinoma Cells.
Article in In vivo (Athens, Greece). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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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.
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Who cites it
5 citing papers in PubMed, 6 citations in OpenAlex.
- mTOR signaling in cholangiocarcinoma: mechanistic insights and therapeutic opportunities.Frontiers in pharmacology · 2026Review
- Pathology and Therapeutic Significance of Fibroblast Growth Factors.Targets (Basel) · 2025Article
- Decoding FGF/FGFR Signaling: Insights into Biological Functions and Disease Relevance.Biomolecules · 2024Review
- Dual blockage of PI3K-mTOR and FGFR induced autophagic cell death in cholangiocarcinoma cells.Heliyon · 2024Article
- Activated FGFR2 signalling as a biomarker for selection of intrahepatic cholangiocarcinoma patients candidate to FGFR targeted therapies.Scientific reports · 2024Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND/
aimIncreasing evidence has revealed FGFR2 as an attractive therapeutic target for cancer including cholangiocarcinoma (CCA). The present study investigated the oncogenic mechanisms by which FGF10 ligand activates FGFR2 in CCA cells and determined whether FGFR inhibitors could suppress FGF10-mediated migration of CCA cells. MATERIALS AND
methodsEffects of FGF10 on the proliferation, migration, and invasion of KKU-M213A cells were assessed using clonogenic and transwell assays. Protein expression levels of FGFR2 and pro-angiogenic factors were determined via immunoblotting and antibody array analysis. FGFR2 knockdown using a small interfering RNA was used to validate the role of FGF10 in promoting cell migration via FGFR2. The effects of infigratinib (FGFR inhibitor) on cell viability, were determined in KKU-100, KKU-M213A, KKU-452 cells. Moreover, the efficacy of the FGFR inhibitor in suppressing migration via FGF10/FGFR2 stimulation was assessed in KKU-M213A cells.
resultsFGF10 significantly increased the expression of phospho-FGFR/FGFR2 and promoted the proliferation, migration, and invasion of KKU-M213A cells. FGF10 increased the expression levels of p-Akt, p-mTOR, VEGF, Slug, and pro-angiogenic proteins related to metastasis. Cell migration mediated by FGF10 was markedly decreased in FGFR2-knockdown cells. Moreover, FGF10/FGFR2 promoted the migration of cells, which was suppressed by the FGFR inhibitor.
conclusionFGF10/FGFR2 activates the Akt/mTOR and VEGF/Slug pathways, which are associated with the stimulation of migration and invasion in CCA. Moreover, the FGF10/FGFR2 signaling was inhibited by an FGFR inhibitor resulting suppression of cell migration, which warrants further studies on their clinical utility for CCA treatment.
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