ArticleThe EMBO journal2019
Inhibition of CPAP-tubulin interaction prevents proliferation of centrosome-amplified cancer cells.
Article in The EMBO journal, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.
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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
20 citing papers in PubMed, 1 synthesis or guideline pooled it, 33 citations in OpenAlex.
- Brain multi-omic Mendelian randomisation to identify novel drug targets for gliomagenesis.Human molecular genetics · 2025Pooled it
- Disrupted STIL-BRCA1 axis causes centrosome amplification and genomic instability.FEBS letters · 2026Article
- ALDH+ Anaplastic Thyroid Cancer Cells Show Vulnerability to a Pharmacologic Inducer of Centrosome Declustering.Cancer research communications · 2026Article
- Cytoplasmic control of spindle architecture.Nature cell biology · 2025Article
- Cell state-specific cytoplasmic density controls spindle architecture and scaling.Nature cell biology · 2025Article
- Identification of a ligand-binding site on tubulin mediating the tubulin-RB3 interaction.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Inhibiting centrosome clustering reduces cystogenesis and improves kidney function in autosomal dominant polycystic kidney disease.JCI insight · 2024Article
- Centrosomes and associated proteins in pathogenesis and treatment of breast cancer.Frontiers in oncology · 2024Review
- Whole-Genome Duplication and Genome Instability in Cancer Cells: Double the Trouble.International journal of molecular sciences · 2023Review
- KIF24 depletion induces clustering of supernumerary centrosomes in PDAC cells.Life science alliance · 2022Article
- 3D-Structured Illumination Microscopy of Centrosomes in Human Cell Lines.Bio-protocol · 2022Article
- Mechanisms involved in selecting and maintaining neuroblastoma cancer stem cell populations, and perspectives for therapeutic targeting.World journal of stem cells · 2021Review
- Mud binds the kinesin-14 Ncd inBiochemistry and biophysics reports · 2021Article
- Loss of CPAP causes sustained EGFR signaling and epithelial-mesenchymal transition in oral cancer.Oncotarget · 2021Article
- Centrosome amplification: a quantifiable cancer cell trait with prognostic value in solid malignancies.Cancer metastasis reviews · 2021Review
- Review
- The Modified Phenanthridine PJ34 Unveils an Exclusive Cell-Death Mechanism in Human Cancer Cells.Cancers · 2020Review
- Targeting centrosome amplification, an Achilles' heel of cancer.Biochemical Society transactions · 2019Review
- Centrosome-derived microtubule radial array, PCM-1 protein, and primary cilia formation.Protoplasma · 2019Article
- A magic bullet for targeting cancers with supernumerary centrosomes.The EMBO journal · 2019Article
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Authors and funding
26 authors at 9 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Centrosome amplification is a hallmark of human cancers that can trigger cancer cell invasion. To survive, cancer cells cluster amplified extra centrosomes and achieve pseudobipolar division. Here, we set out to prevent clustering of extra centrosomes. Tubulin, by interacting with the centrosomal protein CPAP, negatively regulates CPAP-dependent peri-centriolar material recruitment, and concurrently microtubule nucleation. Screening for compounds that perturb CPAP-tubulin interaction led to the identification of CCB02, which selectively binds at the CPAP binding site of tubulin. Genetic and chemical perturbation of CPAP-tubulin interaction activates extra centrosomes to nucleate enhanced numbers of microtubules prior to mitosis. This causes cells to undergo centrosome de-clustering, prolonged multipolar mitosis, and cell death. 3D-organotypic invasion assays reveal that CCB02 has broad anti-invasive activity in various cancer models, including tyrosine kinase inhibitor (TKI)-resistant EGFR-mutant non-small-cell lung cancers. Thus, we have identified a vulnerability of cancer cells to activation of extra centrosomes, which may serve as a global approach to target various tumors, including drug-resistant cancers exhibiting high incidence of centrosome amplification.
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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 Socratic graph.