ArticleChromosoma2013
Abnormal mitosis triggers p53-dependent cell cycle arrest in human tetraploid cells.
Article in Chromosoma, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
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Who cites it
49 citing papers in PubMed, 75 citations in OpenAlex.
- Whole genome duplication through mitotic slippage causes nuclear instability.The EMBO journal · 2026Article
- Chromosomal instability in cancer: sources, consequences and new therapeutic opportunities.Signal transduction and targeted therapy · 2026Review
- Tetraploids or polyploid giants: who is truly dangerous?Trends in cell biology · 2026Review
- The immediate cellular response to whole-genome doubling is conserved across polyploid contexts.bioRxiv : the preprint server for biology · 2026Article
- RSRC2 is a novel RNA-binding protein that safeguards mitotic fidelity by interacting with the lncRNA C1QTNF1-AS1.Nucleic acids research · 2026Article
- LncTRDMT1-5 promotes chromosomal instability through MSRB3-mediated cell cycle and DNA damage in breast cancer.Frontiers in oncology · 2026Article
- The two sides of chromosomal instability: drivers and brakes in cancer.Signal transduction and targeted therapy · 2024Review
- Long noncoding RNA,Frontiers in cell and developmental biology · 2024Article
- Permission to pass: on the role of p53 as a gatekeeper for aneuploidy.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2023Review
- BLM helicase overexpressed in human gliomas contributes to diverse responses of human glioma cells to chemotherapy.Cell death discovery · 2023Article
- Expression of the cytokinesis regulator PRC1 results in p53-pathway activation in A549 cells but does not directly regulate gene expression in the nucleus.Cell cycle (Georgetown, Tex.) · 2023Article
- The fate of extra centrosomes in newly formed tetraploid cells: should I stay, or should I go?Frontiers in cell and developmental biology · 2023Review
- Sublinear scaling of the cellular proteome with ploidy.Nature communications · 2022Article
- Oncogenic BRAF induces whole-genome doubling through suppression of cytokinesis.Nature communications · 2022Article
- Genome doubling causes double trouble.Nature · 2022Article
- Loss of USP28 and SPINT2 expression promotes cancer cell survival after whole genome doubling.Cellular oncology (Dordrecht, Netherlands) · 2022Article
- Christia vespertilionis extract induced antiproliferation and apoptosis in breast cancer (MCF7) cells.Molecular biology reports · 2021Article
- Review
- Context-dependent effects of whole-genome duplication during mammary tumor recurrence.Scientific reports · 2021Article
- Targeting c-IAP1, c-IAP2, and Bcl-2 Eliminates Senescent Glioblastoma Cells Following Temozolomide Treatment.Cancers · 2021Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Erroneously arising tetraploid mammalian cells are chromosomally instable and may facilitate cell transformation. An increasing body of evidence shows that the propagation of mammalian tetraploid cells is limited by a p53-dependent arrest. The trigger of this arrest has not been identified so far. Here we show by live cell imaging of tetraploid cells generated by an induced cytokinesis failure that most tetraploids arrest and die in a p53-dependent manner after the first tetraploid mitosis. Furthermore, we found that the main trigger is a mitotic defect, in particular, chromosome missegregation during bipolar mitosis or spindle multipolarity. Both a transient multipolar spindle followed by efficient clustering in anaphase as well as a multipolar spindle followed by multipolar mitosis inhibited subsequent proliferation to a similar degree. We found that the tetraploid cells did not accumulate double-strand breaks that could cause the cell cycle arrest after tetraploid mitosis. In contrast, tetraploid cells showed increased levels of oxidative DNA damage coinciding with the p53 activation. To further elucidate the pathways involved in the proliferation control of tetraploid cells, we knocked down specific kinases that had been previously linked to the cell cycle arrest and p53 phosphorylation. Our results suggest that the checkpoint kinase ATM phosphorylates p53 in tetraploid cells after abnormal mitosis and thus contributes to proliferation control of human aberrantly arising tetraploids.
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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.