PTEN regulates PLK1 and controls chromosomal stability during cell division
Open accessAbstract
PTEN functions as a guardian of the genome through multiple mechanisms. We have previously established that PTEN maintains the structural integrity of chromosomes. In this report, we demonstrate a fundamental role of PTEN in controlling chromosome inheritance to prevent gross genomic alterations. Disruption of PTEN or depletion of PTEN protein phosphatase activity causes abnormal chromosome content, manifested by enlarged or polyploid nuclei. We further identify polo-like kinase 1 (PLK1) as a substrate of PTEN phosphatase. PTEN can physically associate with PLK1 and reduce PLK1 phosphorylation in a phosphatase-dependent manner. We show that PTEN deficiency leads to PLK1 phosphorylation and that a phospho-mimicking PLK1 mutant causes polyploidy, imitating functional deficiency of PTEN phosphatase. Inhibition of PLK1 activity or overexpression of a non-phosphorylatable PLK1 mutant reduces the polyploid cell population. These data reveal a new mechanism by which PTEN controls genomic stability during cell division.
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PTEN mutation leads to disruption of proper spindle assembly and chromosome segregation, resulting in mitotic catastrophe.
“PTEN mutation leads to disruption of proper spindle assembly and chromosome segregation, which results in mitotic catastrophe [93,94].”
From Permeabilizing Cell Membranes with Electric Fields (2021) · cites this paper as [94]
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References 69 · Cited by 46
- Authors
- Zhang, Z., Hou, S.-Q., He, J., Gu, T., Yin, Y., & Shen, W. H.
- Affiliations
- Cornell University (US)
- Department of Radiation Oncology, Weill Medical Medicine, Cornell University, New York, NY, USA
- Peking University (CN)
- Corresponding author
- Yin, Yuxin
- Shen, Wen H.
- Venue
- Cell Cycle
- Publisher
- Informa UK Limited
- Published
- 2016-08-03
- Volume
- 15
- Issue
- 18
- Pages
- 2476-2485
- ISSN
- 1538-4101 (ISSN-L)
- 1551-4005
- PMC
- PMC5026806
- OpenAlex
- W2474488847
- Cited by
- 46
- References
- 69
- Citations by year
- 2026: 6 · 2025: 3 · 2024: 3 · 2023: 2 · 2022: 8 · 2021: 5 · 2020: 4 · 2019: 3 · 2018: 5 · 2017: 4 · 2016: 3
- FWCI
- 3.44
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Cell Cycle (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Figshare (submittedVersion, cc-by)
- Figshare (cc-by)
- Funders
- National Institutes of Health
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Microtubule and mitosis dynamics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › PI3K/AKT/mTOR signaling in cancer
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Keywords
- PTEN, PLK1, PLK1 phosphorylation, chromosome stability, genome stability, polyploidy, chromosome inheritance, cell division, tumor suppressor
- MeSH terms
- Polo-Like Kinase 1, Animals, Cell Division, Enzyme Activation, Enzyme Stability, HeLa Cells, Humans, Karyotyping, Mitosis, Spindle Apparatus, Phosphorylation, Polyploidy, Proto-Oncogene Proteins, Substrate Specificity, Nocodazole, Protein Serine-Threonine Kinases, Cell Cycle Proteins, Chromosomal Instability, PTEN Phosphohydrolase, Mice
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