ArticleCancer research2009
Fibroblast growth factor receptor 1 promotes proliferation and survival via activation of the mitogen-activated protein kinase pathway in bladder cancer.
Article in Cancer research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers, 1 of them a synthesis that pooled it.
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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
62 citing papers in PubMed, 1 synthesis or guideline pooled it, 137 citations in OpenAlex.
- Safety and efficacy of the pan-FGFR inhibitor erdafitinib in advanced urothelial carcinoma and other solid tumors: A systematic review and meta-analysis.Frontiers in oncology · 2022Pooled it
- Multi-omic profiling defines three distinct molecular subtypes of urothelial carcinoma with implications for precision therapy.Clinical and translational medicine · 2026Article
- Post-translational modifications: Principal regulators of bladder cancer.Molecular biology reports · 2026Review
- Cell-of-origin and genetic drivers define advanced bladder cancer subtypes and potential therapeutic response in mouse models.Journal of experimental & clinical cancer research : CR · 2026Article
- Towards biomarker-driven therapies for urothelial carcinoma.Nature reviews. Clinical oncology · 2026Review
- MET signaling drives acquired resistance to erdafitinib in muscle-invasive bladder cancer cells.Cell death & disease · 2025Article
- Isolation and Comprehensive Analysis of Cochlear Tissue-Derived Small Extracellular Vesicles.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- The roles of FGFR3 and c-MYC in urothelial bladder cancer.Discover oncology · 2024Review
- Article
- Novel dual inhibitor for targeting PIM1 and FGFR1 kinases inhibits colorectal cancer growthActa pharmaceutica Sinica. B · 2022Article
- Review
- Intrinsically Fluorescent Oligomeric Cytotoxic Conjugates Toxic for FGFR1-Overproducing Cancers.Biomacromolecules · 2021Article
- Review
- Apoptotic stress-induced FGF signalling promotes non-cell autonomous resistance to cell death.Nature communications · 2021Article
- The cytotoxic conjugate of highly internalizing tetravalent antibody for targeting FGFR1-overproducing cancer cells.Molecular medicine (Cambridge, Mass.) · 2021Article
- Classification of bladder cancer cell lines according to regulon activity.Turkish journal of biology = Turk biyoloji dergisi · 2021Article
- FGFR1 clustering with engineered tetravalent antibody improves the efficiency and modifies the mechanism of receptor internalization.Molecular oncology · 2020Article
- Fibroblast growth factor receptor signaling as therapeutic targets in female reproductive system cancers.Journal of Cancer · 2020Review
- The prognostic value of six survival-related genes in bladder cancer.Cell death discovery · 2020Article
- Rogaratinib: A potent and selective pan-FGFR inhibitor with broad antitumor activity in FGFR-overexpressing preclinical cancer models.International journal of cancer · 2019Article
2 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Fibroblast growth factor receptors (FGFR) play key roles in proliferation, differentiation, and tumorigenesis. Many urothelial carcinomas contain activating point mutations or increased expression of FGFR3. However, little is known about the role of other FGFRs. We examined FGFR expression in telomerase-immortalized normal human urothelial cells, urothelial carcinoma cell lines, and tumor samples and showed that FGFR1 expression is increased in a high proportion of cell lines and tumors independent of stage and grade. To determine the role of FGFR1 in low-stage bladder cancer, we overexpressed FGFR1 in telomerase-immortalized normal human urothelial cells and examined changes in proliferation and cell survival in response to FGF2. FGFR1 stimulation increased proliferation and reduced apoptosis. To elucidate the mechanistic basis for these alterations, we examined the signaling cascades activated by FGFR1. FRS2alpha and PLCgamma were activated in response to FGF2, leading to activation of the mitogen-activated protein kinase pathway. The level of mitogen-activated protein kinase activation correlated with the level of cyclin D1, MCL1, and phospho-BAD, which also correlated with FGFR-induced proliferation and survival. Knockdown of FGFR1 in urothelial carcinoma cell lines revealed differential FGFR1 dependence. JMSU1 cells were dependent on FGFR1 expression for survival but three other cell lines were not. Two cell lines (JMSU1 and UMUC3) were dependent on FGFR1 for growth in soft agar. Only one of the cell lines tested (UMUC3) was frankly tumorigenic; here, FGFR1 knockdown inhibited tumor growth. Our results indicate that FGFR1 has significant effects on urothelial cell phenotype and may represent a useful therapeutic target in some cases of urothelial carcinoma.
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