ArticleInternational forum of allergy & rhinology2017
Inhibition of fibroblast growth factor receptor with AZD4547 mitigates juvenile nasopharyngeal angiofibroma.
Article in International forum of allergy & rhinology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 10 citations in OpenAlex.
- Molecular Mechanisms of Juvenile Nasopharyngeal Angiofibroma: A Narrative Review.Current oncology (Toronto, Ont.) · 2026Review
- Integrated Molecular and Histological Insights for Targeted Therapies in Mesenchymal Sinonasal Tract Tumors.Current oncology reports · 2024Review
- FGFR3 and FGFR4 overexpression in juvenile nasopharyngeal angiofibroma: impact of smoking history and implications for personalized management.Journal of applied genetics · 2023Article
- [Association between vascularization and its impact for recurrence of juvenile nasoangiofibroma].Revista medica del Instituto Mexicano del Seguro Social · 2023Observational
- Inhibition of CK2 Reduces NG2 Expression in Juvenile Angiofibroma.Biomedicines · 2022Article
- Differential Gene Expression and Pathway Analysis in Juvenile Nasopharyngeal Angiofibroma Using RNA Sequencing.Otolaryngology--head and neck surgery : official journal of American Academy of Otolaryngology-Head and Neck Surgery · 2018Article
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundJuvenile nasopharyngeal angiofibroma (JNA) is a benign tumor that presents in adolescent males. Although surgical excision is the mainstay of treatment, recurrences complicate treatment. There is a need to develop less invasive approaches for management. JNA tumors are composed of fibroblasts and vascular endothelial cells. We identified fibroblast growth factor receptor (FGFR) and vascular endothelial growth factor (VEGF) expression in JNA-derived fibroblasts. FGFR influences fibroblast proliferation and VEGF is necessary for angiogenesis. We hypothesized that targeting FGFR would mitigate JNA fibroblast proliferation, invasion, and migration, and that targeting the VEGF receptor would attenuate endothelial tubule formation.
methodsAfter informed consent, fibroblasts from JNA explants of 3 patients were isolated. Fibroblasts were treated with FGFR inhibitor AZD4547, 0 to 25 μg/mL for 72 hours and proliferation was quantified using CyQuant assay. Migration and invasion of JNA were assessed using 24-hour transwell assays with subsequent fixation and quantification. Mitigation of FGFR and downstream signaling was evaluated by immunoblotting. Tubule formation was assessed in human umbilical vein endothelial cells (HUVECs) treated with vehicle control (dimethylsulfoxide [DMSO]) or semaxanib (SU5416) as well as in serum-free media (SFM) or JNA conditioned media (CM). Tubule length was compared between treatment groups.
resultsCompared to control, AZD4547 inhibited JNA fibroblast proliferation, migration, and invasion through inhibition of FGFR and downstream signaling, specifically phosphorylation of - p44/42 mitogen activated protein kinase (p44/42 MAPK). JNA fibroblast CM significantly increased HUVEC tubule formation (p = 0.0039).
conclusionAZD4547 effectively mitigates FGFR signaling and decreases JNA fibroblast proliferation, migration, and invasion. SU5416 attenuated JNA fibroblast-induced tubule formation. AZD4547 may have therapeutic potential in the treatment of JNA.
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