Proliferation of aneuploid human cells is limited by a p53-dependent mechanism
Open accessAbstract
Most solid tumors are aneuploid, and it has been proposed that aneuploidy is the consequence of an elevated rate of chromosome missegregation in a process called chromosomal instability (CIN). However, the relationship of aneuploidy and CIN is unclear because the proliferation of cultured diploid cells is compromised by chromosome missegregation. The mechanism for this intolerance of nondiploid genomes is unknown. In this study, we show that in otherwise diploid human cells, chromosome missegregation causes a cell cycle delay with nuclear accumulation of the tumor suppressor p53 and the cyclin kinase inhibitor p21. Deletion of the p53 gene permits the accumulation of nondiploid cells such that CIN generates cells with aneuploid genomes that resemble many human tumors. Thus, the p53 pathway plays an important role in limiting the propagation of aneuploid human cells in culture to preserve the diploid karyotype of the population. These data fit with the concordance of aneuploidy and disruption of the p53 pathway in many tumors, but the presence of aneuploid cells in some normal human and mouse tissues indicates that there are known exceptions to the involvement of p53 in aneuploid cells and that tissue context may be important in how cells respond to aneuploidy.
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A post-mitotic response involving activation of the p53 pathway is more likely than alternative explanations for TTFields-induced cell death.
“Thus, a post mitotic response which involves activation of the p53 pathway is more likely6162.”
From Mitotic Spindle Disruption by Alternating Electric Fields Leads to Improper Chromosome Segregation and Mitotic Catastrophe in Cancer Cells (2015) · cites this paper as [61]
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- Authors
- Thompson, S. L., & Compton, D. A.
- Affiliations
- Dartmouth College (US)
- Corresponding author
- Compton, Duane A.
- Venue
- Journal of Cell Biology
- Publisher
- Rockefeller University Press
- Published
- 2010-02-01
- Volume
- 188
- Issue
- 3
- Pages
- 369-381
- ISSN
- 0021-9525 (ISSN-L)
- 1540-8140
- PMC
- PMC2819684
- OpenAlex
- W2102502996
- Cited by
- 494
- References
- 61
- Citations by year
- 2026: 19 · 2025: 28 · 2024: 33 · 2023: 34 · 2022: 26 · 2021: 27 · 2020: 22 · 2019: 26 · 2018: 32 · 2017: 35 · 2016: 37 · 2015: 42 · 2014: 14 · 2013: 42 · 2012: 33
- FWCI
- 16.65
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- cc-by-nc-sa
- Locations
- The Journal of Cell Biology (publishedVersion, cc-by-nc-sa)
- PubMed Central (publishedVersion, cc-by-nc-sa)
- PubMed (publishedVersion)
- Funders
- National Institute of General Medical Sciences (GM51542, R01GM051542, T32GM008704, R37GM051542, GM008704)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Microtubule and mitosis dynamics
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Keywords
- aneuploidy, p53, p21, chromosomal instability, chromosome missegregation, cell proliferation, cell cycle delay, tumor suppressor pathways, diploid karyotype, solid tumors
- MeSH terms
- Aneuploidy, Animals, Chromosomes, Human, Humans, Neoplasms, Tumor Suppressor Protein p53, Chromosomal Instability, Cell Line, Tumor, Cell Proliferation, Mice
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