ArticleBritish journal of cancer2010
Fibroblast growth factor receptor 3-IIIc mediates colorectal cancer growth and migration.
Article in British journal of cancer, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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46 citing papers in PubMed, 79 citations in OpenAlex.
- Unraveling the FGFR-RNA splicing axis: Mechanisms, oncogenic crosstalks and innovations for therapeutic purpose.Acta pharmaceutica Sinica. B · 2026Review
- Rewiring the transcriptome: diagnostic and therapeutic implications of alternative splicing in solid cancers.Molecular biology reports · 2025Review
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- FGFR3 amplification is predictive of poor prognosis in esophageal squamous cell carcinoma patients.Virchows Archiv : an international journal of pathology · 2025Article
- How Driver Oncogenes Shape and Are Shaped by Alternative Splicing Mechanisms in Tumors.Cancers · 2023Review
- The role of fibroblast growth factor 18 in cancers: functions and signaling pathways.Frontiers in oncology · 2023Review
- Broad misappropriation of developmental splicing profile by cancer in multiple organs.Nature communications · 2022Article
- Waldenström Macroglobulinemia: Mechanisms of Disease Progression and Current Therapies.International journal of molecular sciences · 2022Review
- Characterization and clustering of kinase isoform expression in metastatic melanoma.PLoS computational biology · 2022Article
- Targeting fibroblast growth factor receptors to combat aggressive ependymoma.Acta neuropathologica · 2021Article
- Alternative splicing modulates cancer aggressiveness: role in EMT/metastasis and chemoresistance.Molecular biology reports · 2021Review
- Alternative splicing in endothelial cells: novel therapeutic opportunities in cancer angiogenesis.Journal of experimental & clinical cancer research : CR · 2020Review
- Article
- Development of a precision medicine pipeline to identify personalized treatments for colorectal cancer.BMC cancer · 2020Article
- The Expression and Prognostic Value of FGF2, FGFR3, and FGFBP1 in Esophageal Squamous Cell Carcinoma.Analytical cellular pathology (Amsterdam) · 2020Article
- Article
- Article
- Addiction of mesenchymal phenotypes on the FGF/FGFR axis in oral squamous cell carcinoma cells.PloS one · 2019Article
- FGF8 induces therapy resistance in neoadjuvantly radiated rectal cancer.Journal of cancer research and clinical oncology · 2019Article
- Alternative-splicing defects in cancer: Splicing regulators and their downstream targets, guiding the way to novel cancer therapeutics.Wiley interdisciplinary reviews. RNA · 2018Review
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Authors and funding
15 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundDeregulation of fibroblast growth factor receptor 3 (FGFR3) is involved in several malignancies. Its role in colorectal cancer has not been assessed before.
methodsExpression of FGFR3 in human colorectal tumour specimens was analysed using splice variant-specific real-time reverse transcriptase PCR assays. To analyse the impact of FGFR3-IIIc expression on tumour cell biology, colon cancer cell models overexpressing wild-type (WT-3b and WT3c) or dominant-negative FGFR3 variants (KD3c and KD3b) were generated by either plasmid transfection or adenoviral transduction.
resultsAlthough FGFR3 mRNA expression is downregulated in colorectal cancer, alterations mainly affected the FGFR3-IIIb splice variant, resulting in an increased IIIc/IIIb ratio predominantly in a subgroup of advanced tumours. Overexpression of WT3c increased proliferation, survival and colony formation in all colon cancer cell models tested, whereas WT3b had little activity. In addition, it conferred sensitivity to autocrine FGF18-mediated growth and migration signals in SW480 cells with low endogenous FGFR3-IIIc expression. Disruption of FGFR3-IIIc-dependent signalling by dominant-negative FGFR3-IIIc or small interfering RNA-mediated FGFR3-IIIc knockdown resulted in inhibition of cell growth and induction of apoptosis, which could not be observed when FGFR3-IIIb was blocked. In addition, KD3c expression blocked colony formation and migration and distinctly attenuated tumour growth in SCID mouse xenograft models.
conclusionOur data show that FGFR3-IIIc exerts oncogenic functions by mediating FGF18 effects in colorectal cancer and may constitute a promising new target for therapeutic interventions.
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