ArticleMolecular biology of the cell2012
Prolonged mitotic arrest triggers partial activation of apoptosis, resulting in DNA damage and p53 induction.
Article in Molecular biology of the cell, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 153 papers.
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Who cites it
153 citing papers in PubMed, 252 citations in OpenAlex.
- Tumor gasdermin E acts as a rheostat to limit apoptotic cell survival and mutagenesis in anticancer immune environments.Science advances · 2026Article
- Evasion of cell death despite mitochondrial outer membrane permeabilization: an oncogenic outcome of apoptosis.Apoptosis : an international journal on programmed cell death · 2026Review
- Deciphering mitotic catastrophe-associated transcriptomic patterns in renal cell carcinoma: prognostic significance and immunotherapy-related associations.Biology direct · 2026Article
- Therapy-induced senescent cancer cells as bidirectional regulators of antitumor immunity and resistance in the tumor microenvironment.Cell death & disease · 2026Review
- Impact of Chromosomal Instability and Aneuploidy in Cancer Development.Annual review of cancer biology · 2026Article
- Fidelity-Ensuring Consistency of Mitosis is Safeguarded by the 53BP1-USP28-p53 Pathway.bioRxiv : the preprint server for biology · 2026Article
- Protein-only centromeric chromatin assembly streamlines human artificial chromosome formation.bioRxiv : the preprint server for biology · 2026Article
- TMT-based quantitative proteomic assessment of Vicia sativa induced neurotoxicity by β-cyano-L-alanine and γ-glutamyl-β-cyano-L-alanine in SH-SY5Y cells.Scientific reports · 2025Article
- Microbial Metabolite, Macro Impact: Urolithin A in the Nexus of Insulin Resistance and Colorectal Tumorigenesis.Nutrients · 2025Review
- CRO-67 has anti-cancer activity in pancreatic tumor cells and stromal cancer-associated fibroblasts.Scientific reports · 2025Article
- A Novel HDAC6 Inhibitor Enhances the Efficacy of Paclitaxel Against Ovarian Cancer Cells.Molecules (Basel, Switzerland) · 2025Article
- Suppression of global protein synthesis and hepatocellular carcinoma cell growth by Benzimidazoisoquinoline, 4,11-Dichloro-BBQ.Biochemical pharmacology · 2025Article
- A CPC-shelterin-BTR axis regulates mitotic telomere deprotection.Nature communications · 2025Article
- Caspase 3 and caspase 7 promote cytoprotective autophagy and the DNA damage response during non-lethal stress conditions in human breast cancer cells.PLoS biology · 2025Article
- Factors that determine cell fate in mitotically arrested cancer cells.Frontiers in cell and developmental biology · 2025Article
- miR-31-mediated local translation at the mitotic spindle is important for early development.Development (Cambridge, England) · 2024Article
- Mitochondria and cell death.Nature cell biology · 2024Review
- The caspase-activated DNase promotes cellular senescence.The EMBO journal · 2024Article
- Chromosomal instability in a patient with ring chromosome 14 syndrome: a case report.Molecular cytogenetics · 2024Article
- MicroRNA‑155‑5p inhibits trophoblast cell proliferation and invasion by disrupting centrosomal function.Molecular medicine reports · 2024Article
93 more citing papers are in PubMed but not listed here.
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Mitotic arrest induced by antimitotic drugs can cause apoptosis or p53-dependent cell cycle arrest. It can also cause DNA damage, but the relationship between these events has been unclear. Live, single-cell imaging in human cancer cells responding to an antimitotic kinesin-5 inhibitor and additional antimitotic drugs revealed strong induction of p53 after cells slipped from prolonged mitotic arrest into G1. We investigated the cause of this induction. We detected DNA damage late in mitotic arrest and also after slippage. This damage was inhibited by treatment with caspase inhibitors and by stable expression of mutant, noncleavable inhibitor of caspase-activated DNase, which prevents activation of the apoptosis-associated nuclease caspase-activated DNase (CAD). These treatments also inhibited induction of p53 after slippage from prolonged arrest. DNA damage was not due to full apoptosis, since most cytochrome C was still sequestered in mitochondria when damage occurred. We conclude that prolonged mitotic arrest partially activates the apoptotic pathway. This partly activates CAD, causing limited DNA damage and p53 induction after slippage. Increased DNA damage via caspases and CAD may be an important aspect of antimitotic drug action. More speculatively, partial activation of CAD may explain the DNA-damaging effects of diverse cellular stresses that do not immediately trigger apoptosis.
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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 OpenQuestion graph.