ArticleMolecular cancer2025
Targeting FGFR4 abrogates HNF1A-driven metastasis in pancreatic ductal adenocarcinoma.
Article in Molecular cancer, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Dual Targeting of FGFR4 and PI3K-mTOR Suppresses Tumor-Associated Phenotypes in Pancreatic Ductal Adenocarcinoma.International journal of molecular sciences · 2026Article
- METTL3-Modified FOXM1 Promotes Proliferation, Invasion, Stemness, and Immune Escape of Gastric Cancer by Influencing the Transcription of FGFR4.Applied biochemistry and biotechnology · 2026Article
- Construction of a prognostic risk model based on colorectal cancer-specific ferroptosis genes and preliminary validation of FGFR4.Translational cancer research · 2026Article
- High FGFR4 protein expression, but not FGFR1 or FGFR2, predicts poor prognosis in pancreatic ductal adenocarcinoma.BMC cancer · 2025Article
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Abstract
backgroundWe previously identified an oncogenic role for the transcription factor HNF1A in pancreatic ductal adenocarcinoma (PDAC). However, the role of HNF1A in the metastatic progression of PDAC remains unknown and targeting modalities for HNF1A-dependent phenotypes have yet to be identified.
methodsTranswell chambers were used to assess the effects of HNF1A and FGFR4 modulation on the migration and invasion of ATCC and patient-derived PDAC cells in vitro. An intrasplenic injection xenograft model was used to evaluate the impact of HNF1A knockdown and overexpression on metastatic tumor burden. Single-cell RNA sequencing (scRNA-seq), tissue microarray (TMA) data, and UMAP spatial profiling were used to identify FGFR4 as an HNF1A target gene upregulated in metastatic cells. RNAi and two FGFR4 inhibiting modalities (H3B-6527 and U3-1784) were utilized to demonstrate the efficacy of FGFR4 inhibiting agents at reducing HNF1A-driven metastasis.
resultsKnockdown of HNF1A significantly decreases and HNF1A overexpression significantly increases PDAC cell migration and invasion. In vivo studies show that HNF1A knockdown significantly abrogates metastasis, while overexpression significantly promotes metastasis. scRNA-seq shows that FGFR4 is upregulated in metastatic PDAC cells and staining for HNF1A and FGFR4 in a PDAC TMA reveals significant correlation between HNF1A and FGFR4 in PDAC patients. Further, knockdown and inhibition of FGFR4 significantly decreases HNF1A-mediated cell migration and invasion, and blocks HNF1A-driven metastasis in vivo.
conclusionsThese findings demonstrate that HNF1A drives PDAC metastasis via upregulation of FGFR4, and FGFR4 inhibition is a potential mechanism to target metastasis in PDAC patients.
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