ArticleOncotarget2014
The Aurora-A inhibitor MLN8237 affects multiple mitotic processes and induces dose-dependent mitotic abnormalities and aneuploidy.
Article in Oncotarget, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 49 citations in OpenAlex.
- Multinucleation and cytotoxicity induced by multikinase inhibition in highly proliferative cells.Journal of toxicologic pathology · 2026Article
- The ATC12 small molecule inhibits the Aurora-A/TPX2 interaction and impairs the proliferation of breast cancer cells.Cell death & disease · 2026Article
- AURKA modulates tight junction functionality to influence the proliferation and metastasis of lung adenocarcinoma.Molecular and cellular biochemistry · 2026Article
- The dynamics of ciliogenesis in prepubertal mouse meiosis reveals new clues about testis maturation.Frontiers in cell and developmental biology · 2026Article
- Targeting asymmetric division in cancer stem cells: implications for relapse and resistance.Cancer cell international · 2025Review
- Aurora A regulates the material property of spindle poles to orchestrate nuclear organization at mitotic exit.The EMBO journal · 2025Article
- Functional Profiling of p53 and RB Cell Cycle Regulatory Proficiency Suggests Mechanism-Driven Molecular Stratification in Endometrial Carcinoma.Cancer research communications · 2025Article
- Aurora B inhibition induces hyper-polyploidy and loss of long-term proliferative potential in RB and p53 defective cells.Cell death & disease · 2025Article
- Aurora B inhibitors promote RB hypophosphorylation and senescence independent of p53-dependent CDK2/4 inhibition.Cell death & disease · 2024Article
- ALFI: Cell cycle phenotype annotations of label-free time-lapse imaging data from cultured human cells.Scientific data · 2023Article
- AMBRA1 phosphorylation by CDK1 and PLK1 regulates mitotic spindle orientation.Cellular and molecular life sciences : CMLS · 2023Article
- Identification of Inhibitors of Tubulin Polymerization Using a CRISPR-Edited Cell Line with Endogenous Fluorescent Tagging of β-Tubulin and Histone H1.Biomolecules · 2023Article
- Nuclear localisation of Aurora-A: its regulation and significance for Aurora-A functions in cancer.Oncogene · 2021Review
- Selective targeting of non-centrosomal AURKA functions through use of a targeted protein degradation tool.Communications biology · 2021Article
- Article
- Engineering and combining oncolytic measles virus for cancer therapy.Cytokine & growth factor reviews · 2020Review
- AURKA destruction is decoupled from its activity at mitotic exit but is essential to suppress interphase activity.Journal of cell science · 2020Article
- Article
- A Theoretical Model for the Cell Cycle and Drug Induced Cell Cycle Arrest of FUCCI Systems with Cell-to-Cell Variation during Mitosis.Pharmaceutical research · 2019Article
- A phase 1, first-in-human study of AMG 900, an orally administered pan-Aurora kinase inhibitor, in adult patients with advanced solid tumors.Investigational new drugs · 2018Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Inhibition of Aurora kinase activity by small molecules is being actively investigated as a potential anti-cancer strategy. A successful therapeutic use of Aurora inhibitors relies on a comprehensive understanding of the effects of inactivating Aurora kinases on cell division, a challenging aim given the pleiotropic roles of those kinases during mitosis. Here we have used the Aurora-A inhibitor MLN8237, currently under phase-I/III clinical trials, in dose-response assays in U2OS human cancer cells synchronously proceeding towards mitosis. By following the behaviour and fate of single Aurora-inhibited cells in mitosis by live microscopy, we show that MLN8237 treatment affects multiple processes that are differentially sensitive to the loss of Aurora-A function. A role of Aurora-A in controlling the orientation of cell division emerges. MLN8237 treatment, even in high doses, fails to induce efficient elimination of dividing cells, or of their progeny, while inducing significant aneuploidy in daughter cells. The results of single-cell analyses show a complex cellular response to MLN8237 and evidence that its effects are strongly dose-dependent: these issues deserve consideration in the light of the design of strategies to kill cancer cells via inhibition of Aurora kinases.
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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.