ArticleMolecular medicine reports2019
Deficiency of PTEN leads to aberrant chromosome segregation through downregulation of MAD2.
Article in Molecular medicine reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed, 4 citations in OpenAlex.
- Phospho PTEN mediated dephosphorylation of mitotic kinase PLK1 and Aurora Kinase A prevents aneuploidy and preserves genomic stability.Medical oncology (Northwood, London, England) · 2023Article
- Whole-Exome Sequencing Reveals Recurrent but Heterogeneous Mutational Profiles in Sporadic WHO Grade 1 Meningiomas.Frontiers in oncology · 2021Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Proper spindle formation and accurate chromosome segregation are essential for ensuring mitotic fidelity. Phosphatase and tensin homolog (PTEN) is a multifunctional protein, which is able to maintain the stability of the genome and chromosomes. The present study described an essential role of PTEN in regulating chromosome segregation to prevent gross genomic instability via regulation of mitotic arrest deficient 2 (MAD2). PTEN knockdown induced cell cycle arrest and abnormal chromosome segregation, which manifested as the formation of anaphase bridges, lagging chromosomes and premature chromatid separation. In addition, MAD2 was identified as a potential target of PTEN. Furthermore, the present study revealed that PTEN knockdown resulted in MAD2 degradation via the ubiquitin‑proteasomal pathway, while restoration of MAD2 expression partially ameliorated the mitotic defects induced by PTEN loss. The results from the present study proposed a novel mechanism by which PTEN maintains chromosome stability.
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