ArticlePLoS genetics2015
FGFR3 Deficiency Causes Multiple Chondroma-like Lesions by Upregulating Hedgehog Signaling.
Article in PLoS genetics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 49 citations in OpenAlex.
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- Growth Plate Skeletal Stem Cells and Their Actions Within the Stem Cell Niche.International journal of molecular sciences · 2025Review
- Advances in the mechanism and therapies of achondroplasia.Genes & diseases · 2025Review
- Challenges of engineering a functional growth plateFrontiers in bioengineering and biotechnology · 2025Review
- Identification of a novel splice site mutation in the DNAAF4 gene of a Chinese patient with primary ciliary dyskinesia.Asian journal of andrology · 2023Article
- Exogenous Indian hedgehog antagonist damages intervertebral discs homeostasis in adult mice.Journal of orthopaedic translation · 2022Article
- Review
- Cranial Base Synchondrosis: Chondrocytes at the Hub.International journal of molecular sciences · 2022Review
- Case Report:Frontiers in genetics · 2022Article
- Role of Primary Cilia in Skeletal Disorders.Stem cells international · 2022Review
- SHP-2 deletion in CD4Cre expressing chondrocyte precursors leads to tumor development with wrist tropism.Scientific reports · 2021Article
- Review
- Enchondromatosis and Growth Plate Development.Current osteoporosis reports · 2021Review
- Identification of Two NovelPharmacogenomics and personalized medicine · 2021Article
- FGF/FGFR signaling in health and disease.Signal transduction and targeted therapy · 2020Review
- FGFR3 signaling and function in triple negative breast cancer.Cell communication and signaling : CCS · 2020Article
- Article
- Growth Plate Chondrocytes: Skeletal Development, Growth and Beyond.International journal of molecular sciences · 2019Review
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Authors and funding
14 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Most cartilaginous tumors are formed during skeletal development in locations adjacent to growth plates, suggesting that they arise from disordered endochondral bone growth. Fibroblast growth factor receptor (FGFR)3 signaling plays essential roles in this process; however, the role of FGFR3 in cartilaginous tumorigenesis is not known. In this study, we found that postnatal chondrocyte-specific Fgfr3 deletion induced multiple chondroma-like lesions, including enchondromas and osteochondromas, adjacent to disordered growth plates. The lesions showed decreased extracellular signal-regulated kinase (ERK) activity and increased Indian hedgehog (IHH) expression. The same was observed in Fgfr3-deficient primary chondrocytes, in which treatment with a mitogen-activated protein kinase (MEK) inhibitor increased Ihh expression. Importantly, treatment with an inhibitor of IHH signaling reduced the occurrence of chondroma-like lesions in Fgfr3-deficient mice. This is the first study reporting that the loss of Fgfr3 function leads to the formation of chondroma-like lesions via downregulation of MEK/ERK signaling and upregulation of IHH, suggesting that FGFR3 has a tumor suppressor-like function in chondrogenesis.
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