ArticleCell cycle (Georgetown, Tex.)2016
A novel role for the deubiquitinase USP1 in the control of centrosome duplication.
Article in Cell cycle (Georgetown, Tex.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 12 citations in OpenAlex.
- Centrosome amplification: a quantifiable cancer cell trait with prognostic value in solid malignancies.Cancer metastasis reviews · 2021Review
- UAF1 deubiquitinase complexes facilitate NLRP3 inflammasome activation by promoting NLRP3 expression.Nature communications · 2020Article
- ATAD5 suppresses centrosome over-duplication by regulating UAF1 and ID1.Cell cycle (Georgetown, Tex.) · 2020Article
- USP1 Maintains the Survival of Liver Circulating Tumor Cells by Deubiquitinating and Stabilizing TBLR1.Frontiers in oncology · 2020Article
- Aberrant Activation of β-Catenin Signaling Drives Glioma Tumorigenesis via USP1-Mediated Stabilization of EZH2.Cancer research · 2019Article
- Regulation of the cell cycle and centrosome biology by deubiquitylases.Biochemical Society transactions · 2017Review
- The X-linked deubiquitinase USP9X is an integral component of centrosome.The Journal of biological chemistry · 2017Article
- USP9X regulates centrosome duplication and promotes breast carcinogenesis.Nature communications · 2017Article
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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
Defects in the regulation of centrosome duplication lead to tumorigenesis through abnormal cell division and resulting chromosome missegregation. Therefore, maintenance of accurate centrosome number is critical for cell fate. The deubiquitinating enzyme USP1 plays important roles in DNA repair and cell differentiation. Importantly, increased levels of USP1 are detected in certain types of human cancer, but little is known about the significance of USP1 overexpression in cancer development. Here we show that Usp1 plays a novel role in regulating centrosome duplication. The ectopic expression of wild-type Usp1, but not C90S Usp1 (catalytically inactive mutant form), induced centrosome amplification. Conversely, ablation of Usp1 in mouse embryonic fibroblasts (MEFs) showed a significant delay in centrosome duplication. Moreover, Usp1-induced centrosome amplification caused abnormal mitotic spindles, chromosome missegregation and aneuploidy. Interestingly, loss of inhibitor of DNA binding protein 1 (ID1) suppressed Usp1-induced centrosome amplification. Taken together, our results strongly suggest that Usp1 is involved in the regulation of centrosome duplication, at least in part via ID1, and Usp1 may exert its oncogenic activity, partially through inducing centrosome abnormality.
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