ArticleScientific reports2017
Mitotic slippage and the subsequent cell fates after inhibition of Aurora B during tubulin-binding agent-induced mitotic arrest.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 40 citations in OpenAlex.
- Survivin and Aurora Kinase A control cell fate decisions during mitosis.Molecular oncology · 2026Article
- Isoxazole-Based Compounds Targeting the Taxane-Binding Site of Tubulin.Archiv der Pharmazie · 2025Article
- The immunotoxin targeting PRLR increases tamoxifen sensitivity and enhances the efficacy of chemotherapy in breast cancer.Journal of experimental & clinical cancer research : CR · 2024Article
- Overcoming Clinical Resistance to EZH2 Inhibition Using Rational Epigenetic Combination Therapy.Cancer discovery · 2024Article
- Coupling Kinesin Spindle Protein and Aurora B Inhibition with Apoptosis Induction Enhances Oral Cancer Cell Killing.Cancers · 2024Article
- Regulatory miRNAs, circRNAs and lncRNAs in cell cycle progression of breast cancer.Functional & integrative genomics · 2023Review
- Inhibition of branched-chain alpha-keto acid dehydrogenase kinase augments the sensitivity of ovarian and breast cancer cells to paclitaxel.British journal of cancer · 2023Article
- The deubiquitinating enzyme complex BRISC regulates Aurora B activation via lysine-63-linked ubiquitination in mitosis.Communications biology · 2022Article
- CDC20-Mediated hnRNPU Ubiquitination Regulates Chromatin Condensation and Anti-Cancer Drug Response.Cancers · 2022Article
- Article
- BRAF Inhibitor Resistance Confers Increased Sensitivity to Mitotic Inhibitors.Frontiers in oncology · 2022Article
- Bcl-xL activity influences outcome of the mitotic arrest.Frontiers in pharmacology · 2022Article
- Review
- Predicting cell health phenotypes using image-based morphology profiling.Molecular biology of the cell · 2021Article
- The tyrosine kinase v-Src modifies cytotoxicities of anticancer drugs targeting cell division.Journal of cellular and molecular medicine · 2021Article
- Amentoflavone triggers cell cycle G2/M arrest by interfering with microtubule dynamics and inducing DNA damage in SKOV3 cells.Oncology letters · 2020Article
- Review
- Article
- Aurora B kinase as a therapeutic target in acute lymphoblastic leukemia.Cancer chemotherapy and pharmacology · 2020Article
- The balance between mitotic death and mitotic slippage in acute leukemia: a new therapeutic window?Journal of hematology & oncology · 2019Review
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tubulin-binding agents (TBAs) are designed to target microtubule (MT) dynamics, resulting in compromised mitotic spindles and an unsatisfied spindle assembly checkpoint. The activity of Aurora B kinase is indispensable for TBA-induced mitotic arrest, and its inhibition causes mitotic slippage and postmitotic endoreduplication. However, the precise phenomenon underlying mitotic slippage, which is caused by treatment with both Aurora B inhibitors and TBAs, and the cell fate after postmitotic slippage are not completely understood. Here, we found that HeLa and breast cancer cells treated with the different types of TBAs, such as paclitaxel and eribulin (MT-stabilizing and MT-destabilizing agents, respectively), exhibited distinct behaviors of mitotic slippage on inhibition of Aurora B. In such conditions, the cell fates after postmitotic slippage vastly differed with respect to cell morphology, cell proliferation, and cytotoxicity in short-term culture; that is, the effects of inhibition of Aurora B were beneficial for cytotoxicity enhancement in eribulin treatment but not in paclitaxel. However, in long-term culture, the cells that survived after mitotic slippage underwent endoreduplication and became giant cells in both cases, resulting in cellular senescence. We propose that MT-destabilizing agents may be more appropriate than MT-stabilizing agents for treating cancer cells with a weakened Aurora B kinase activity.
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