ArticleThe American journal of pathology2010
Altered splicing of FGFR1 is associated with high tumor grade and stage and leads to increased sensitivity to FGF1 in bladder cancer.
Article in The American journal of pathology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
37 citing papers in PubMed, 68 citations in OpenAlex.
- Unraveling the FGFR-RNA splicing axis: Mechanisms, oncogenic crosstalks and innovations for therapeutic purpose.Acta pharmaceutica Sinica. B · 2026Review
- Article
- FGF19 in Solid Tumors: Molecular Mechanisms, Metabolic Reprogramming, and Emerging Therapeutic Opportunities.Theranostics · 2026Review
- Targeting Cancer-Associated Fibroblasts in Prostate Cancer: Recent Advances and Therapeutic Opportunities.Cancers · 2025Review
- Characterization of cancer-related fibroblasts in bladder cancer and construction of CAFs-based bladder cancer classification: insights from single-cell and multi-omics analysis.Frontiers in immunology · 2025Article
- Integrating Genetic Alterations and Histopathological Features for Enhanced Risk Stratification in Non-Muscle-Invasive Bladder Cancer.Diagnostics (Basel, Switzerland) · 2024Article
- The roles of FGFR3 and c-MYC in urothelial bladder cancer.Discover oncology · 2024Review
- Bladder cancer.Nature reviews. Disease primers · 2023Review
- N-glycosylation acts as a switch for FGFR1 trafficking between the plasma membrane and nuclear envelope.Cell communication and signaling : CCS · 2023Article
- Biological and clinical implications of FGFR aberrations in paediatric and young adult cancers.Oncogene · 2023Review
- How Driver Oncogenes Shape and Are Shaped by Alternative Splicing Mechanisms in Tumors.Cancers · 2023Review
- Intracellular FGF1 promotes invasion and migration in thyroid carcinoma via HMGA1 independent of FGF receptors.Endocrine connections · 2023Article
- Protein Interactome Profiling of Stable Molecular Complexes in Biomaterial Lysate.International journal of molecular sciences · 2022Review
- Fibroblast Growth Factor Receptor 1 Drives the Metastatic Progression of Prostate Cancer.European urology oncology · 2022Article
- Review
- DDX41 regulates the expression and alternative splicing of genes involved in tumorigenesis and immune response.Oncology reports · 2021Article
- Targeting Splicing Factor SRSF6 for Cancer Therapy.Frontiers in cell and developmental biology · 2021Review
- Current Strategies and Novel Therapeutic Approaches for Metastatic Urothelial Carcinoma.Cancers · 2020Review
- Review
- Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Fibroblast growth factor receptors (FGFRs) play key roles in proliferation, differentiation, and tumorigenesis. Previously, we demonstrated that FGFR1 expression is increased in urothelial carcinoma cell lines and tumors, which promotes proliferation and survival via activation of the mitogen-activated protein kinase (MAPK) pathway. Here we examined splice variants of FGFR1 in both urothelial carcinoma cell lines and tumors. Two known FGFR1 IIIc splice variants (FGFR1α and FGFR1β) were expressed. FGFR1β lacks exon 3 of FGFR1α, removing the first Ig loop of the extracellular domain. Both isoforms were expressed at similar levels in normal urothelial cells, but FGFR1β was expressed at higher levels in most tumor cell lines. In tumor tissues, expression levels were higher than in controls, and the FGFR1β:FGFR1α ratio was significantly increased in association with tumor stage and grade. When FGFR1α and FGFR1β were expressed in urothelial cells, no differences in signaling were observed. FGFR1-induced proliferation paralleled MAPK pathway activation. The relative activation of FGFR1β and FGFR1α by all known mammalian FGFs was examined. Both isoforms were activated by the same FGFs, but the level of activation differed. FGFR1β showed higher affinity for low concentrations of FGF1, leading to enhanced signaling and increased proliferation. An FGFR1α-to-FGFR1β isoform switch and increased FGF1-induced activation of FGFR1β may result in a proliferative advantage that plays a key role during bladder tumor progression.
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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.