ArticleCell cycle (Georgetown, Tex.)2016
Paclitaxel-induced aberrant mitosis and mitotic slippage efficiently lead to proliferative death irrespective of canonical apoptosis and p53.
Article in Cell cycle (Georgetown, Tex.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 35 citations in OpenAlex.
- Assessment of pharmacodynamic interactions of two-drug combinations of five selected cytostatics in an in vitro model of human melanoma: an isobolographic analysis.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Alginate coated mesoporous silica nanoparticles as oral delivery carrier of curcumin and quercetin to colon cancer: preparation, optimization, characterization, and anticancer activity.Drug delivery and translational research · 2025Article
- Kinesin Spindle Protein (KIF11) in Mitosis and Cancer.International journal of molecular sciences · 2025Review
- Emerging phytochemical-based nanocarriers: redefining the perspectives of breast cancer therapy.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- P53 independent pathogenic mechanisms contribute to BubR1 microcephaly.Frontiers in cell and developmental biology · 2023Article
- Bcl-xL activity influences outcome of the mitotic arrest.Frontiers in pharmacology · 2022Article
- Tinker, Tailor, Tumour Suppressor: The Many Functions of PRP4K.Frontiers in genetics · 2022Review
- The effect of paclitaxel on apoptosis, autophagy and mitotic catastrophe in AGS cells.Scientific reports · 2021Article
- Article
- Current Perspectives on Taxanes: Focus on Their Bioactivity, Delivery and Combination Therapy.Plants (Basel, Switzerland) · 2021Review
- Methanolic Fenugreek Seed Extract Induces p53-Dependent Mitotic Catastrophe in Breast Cancer Cells, Leading to Apoptosis.Journal of inflammation research · 2021Article
- Pharmacodynamic modeling of synergistic birinapant/paclitaxel interactions in pancreatic cancer cells.BMC cancer · 2020Article
- BioID-based proteomic analysis of the Bid interactome identifies novel proteins involved in cell-cycle-dependent apoptotic priming.Cell death & disease · 2020Article
- Paclitaxel Potentiates the Anticancer Effect of Cetuximab by Enhancing Antibody-Dependent Cellular Cytotoxicity on Oral Squamous Cell Carcinoma Cells In Vitro.International journal of molecular sciences · 2020Article
- Review
- Role of Bcl-2 on drug resistance in breast cancer polyploidy-induced spindle poisons.Oncology letters · 2020Article
- Stilbene Compounds Inhibit Tumor Growth by the Induction of Cellular Senescence and the Inhibition of Telomerase Activity.International journal of molecular sciences · 2019Review
- Nearly complete deletion of BubR1 causes microcephaly through shortened mitosis and massive cell death.Human molecular genetics · 2019Article
- Observational
- Mapping Mitotic Death: Functional Integration of Mitochondria, Spindle Assembly Checkpoint and Apoptosis.Frontiers in cell and developmental biology · 2018Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Spindle poisons elicit various cellular responses following metaphase arrest, but how they relate to long-term clonogenicity has remained unclear. We prepared several HeLa lines in which the canonical apoptosis pathway was attenuated, and compared their acute responses to paclitaxel, as well as long-term fate, with the parental line. Three-nanomolar paclitaxel induced brief metaphase arrest (<5 h) often followed by aberrant mitosis, and about 90% of the cells of each line had lost their clonogenicity after 48 h of the treatment. A combination of the same concentration of paclitaxel with the kinesin-5 inhibitor, S-trityl-L-cysteine (STLC), at 1 µM led to much longer arrest (∼20 h) and predominance of subsequent line-specific responses: mitochondrial outer membrane permeabilization (MOMP) in the apoptosis-prone line, or mitotic slippage without obvious MOMP in the apoptosis-reluctant lines. In spite of this, combination with STLC did not lead to a marked difference in clonogenicity between the apoptosis-prone and -reluctant lines, and intriguingly resulted in slightly better clonogenicity than that of cells treated with 3 nM paclitaxel alone. This indicates that changes in the short-term response within 3 possible scenarios - acute MOMP, mitotic slippage or aberrant mitosis - has only a weak impact on clonogenicity. Our results suggest that once cells have committed to slippage or aberrant mitosis they eventually undergo proliferative death irrespective of canonical apoptosis or p53 function. Consistent with this, cells with irregular DNA contents originating from mitotic slippage or aberrant mitosis were mostly eliminated from the population within several rounds of division after the drug treatment.
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