ArticleOpen biology2017
FGFR3-TACC3 cancer gene fusions cause mitotic defects by removal of endogenous TACC3 from the mitotic spindle.
Article in Open biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 30 citations in OpenAlex.
- Clinical and Genetic Landscape of Glioblastoma, IDH-Wildtype With FGFR Gene Family Alterations.Cancer science · 2026Article
- Human Papillomavirus Integration Induces Oncogenic Host Gene Fusions in Oropharyngeal Cancers.Cancer discovery · 2025Article
- FGFR inhibitors promote the autophagic degradation of IFN-γ-induced PD-L1 and alleviate the PD-L1-mediated transcriptional suppression of FGFR3-TACC3 in non-muscle-invasive bladder cancer.Cell death & disease · 2025Article
- FGFR3::TACC3 fusions in head and neck carcinomas: a study of nine cases highlighting phenotypic heterogeneity, frequent HPV association, and a morphologically distinct subset in favor of a putative entity.Virchows Archiv : an international journal of pathology · 2025Article
- Syncope in Migraine: A Genome-Wide Association Study Revealing Distinct Genetic Susceptibility Variants Across Subtypes.Journal of clinical neurology (Seoul, Korea) · 2024Article
- Clinicopathological and Molecular Characteristics ofBiomedicines · 2024Article
- Diffuse Gliomas with FGFR3-TACC3 Fusions: Oncogenic Mechanisms, Hallmarks, and Therapeutic Perspectives.Cancers · 2023Review
- Incidental detection of FGFR3 fusion via liquid biopsy leading to earlier diagnosis of urothelial carcinoma.NPJ precision oncology · 2023Article
- Oncogenic driver FGFR3-TACC3 requires five coiled-coil heptads for activation and disulfide bond formation for stability.Oncotarget · 2023Article
- HSP90-CDC37 functions as a chaperone for the oncogenic FGFR3-TACC3 fusion.Molecular therapy : the journal of the American Society of Gene Therapy · 2022Article
- Review
- Clinically relevant fusion oncogenes: detection and practical implications.Therapeutic advances in medical oncology · 2022Review
- Review
- Review
- Genetic and epigenetic landscape of IDH-wildtype glioblastomas with FGFR3-TACC3 fusions.Acta neuropathologica communications · 2020Article
- Whole-exome sequencing reveals potential mechanisms of drug resistance to FGFR3-TACC3 targeted therapy and subsequent drug selection: towards a personalized medicine.BMC medical genomics · 2020Article
- Investigating the impact of the phosphorylation status of tyrosine residues within the TACC domain of TACC3 on microtubule behavior during axon growth and guidance.Cytoskeleton (Hoboken, N.J.) · 2020Article
- FGFR3 signaling and function in triple negative breast cancer.Cell communication and signaling : CCS · 2020Article
- Fibroblast growth factor receptors as treatment targets in clinical oncology.Nature reviews. Clinical oncology · 2019Review
- Oncogenic driver FGFR3-TACC3 is dependent on membrane trafficking and ERK signaling.Oncotarget · 2018Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 2 countries.
Funding
Abstract
Fibroblast growth factor receptor 3-transforming acidic coiled-coil containing protein 3 (FGFR3-TACC3; FT3) is a gene fusion resulting from rearrangement of chromosome 4 that has been identified in many cancers including those of the urinary bladder. Altered FGFR3 signalling in FT3-positive cells is thought to contribute to cancer progression. However, potential changes in TACC3 function in these cells have not been explored. TACC3 is a mitotic spindle protein required for accurate chromosome segregation. Errors in segregation lead to aneuploidy, which can contribute to cancer progression. Here we show that FT3-positive bladder cancer cells have lower levels of endogenous TACC3 on the mitotic spindle, and that this is sufficient to cause mitotic defects. FT3 is not localized to the mitotic spindle, and by virtue of its TACC domain, recruits endogenous TACC3 away from the spindle. Knockdown of the fusion gene or low-level overexpression of TACC3 partially rescues the chromosome segregation defects in FT3-positive bladder cancer cells. This function of FT3 is specific to TACC3 as inhibition of FGFR3 signalling does not rescue the TACC3 level on the spindle in these cancer cells. Models of FT3-mediated carcinogenesis should, therefore, include altered mitotic functions of TACC3 as well as altered FGFR3 signalling.
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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.