ArticleCell cycle (Georgetown, Tex.)2018
Chromosome instability in tumor cells due to defects in Aurora B mediated error correction at kinetochores.
Article in Cell cycle (Georgetown, Tex.), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 15 citations in OpenAlex.
- Single-Cell RNA-Seq Reveals Chromosomal Instability-Associated Transcriptomic Profiles in Breast Cancer.Biomedicines · 2026Article
- RB dependent transcriptional regulation at mitotic centromeres preserves genome stability.Life science alliance · 2026Article
- Suppression of Chromosome Instability Limits Acquired Drug Resistance.Molecular cancer therapeutics · 2022Article
- Polyploid giant cancer cells and ovarian cancer: new insights into mitotic regulators and polyploidy†.Biology of reproduction · 2021Review
- Suv420 enrichment at the centromere limits Aurora B localization and function.Journal of cell science · 2021Article
- The CINs of Polo-Like Kinase 1 in Cancer.Cancers · 2020Review
- Aurora kinases in ovarian cancer.ESMO open · 2020Review
- Untangling the contribution of Haspin and Bub1 to Aurora B function during mitosis.The Journal of cell biology · 2020Article
- Clinical Implications of Chromosomal Instability (CIN) and Kinetochore Abnormalities in Breast Cancers.Molecular diagnosis & therapy · 2019Review
- Where is the right path heading from the centromere to spindle microtubules?Cell cycle (Georgetown, Tex.) · 2019Review
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
We characterized a panel of cancer cells and found that they exhibited chromosome instability (CIN) that was associated with high frequencies of aberrant kinetochore:microtubule attachments. Failure to resolve these defective attachments before anaphase onset can lead to missegregation of chromosomes. Aurora B kinase is concentrated at the inner centromere where it contributes to multiple kinetochore functions, one of which is in error-correction. Analysis of several CIN cell lines showed that many aspects of Aurora B kinase functions were normal. Furthermore, the amount and activity of Aurora B kinase was not reduced at the kinetochores of CIN cells that were examined. However, phosphorylation of a centromeric biosensor for Aurora B in OVCAR10, MCF7 and U2OS cells was consistently reduced relative to non CIN cells. This suggested a localized problem with Aurora B's ability to phosphorylate substrates important for error correction. This possibility was supported by our ability to improve error correction and reduce the frequency of lagging chromosome in CIN cells by directing endogenous Aurora B to the region of centromere that was tested by the biosensor. Our studies suggest that the kinetochores of CIN cells have a defect that limits accessibility of Aurora B to substrates that are important for error-correction.
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Registered trials
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