ArticleTranslational oncology2023
USP39-mediated deubiquitination of Cyclin B1 promotes tumor cell proliferation and glioma progression.
Article in Translational oncology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 17 citations in OpenAlex.
- An unsupervised tool for biomarker discovery and cancer subtyping applied to glioblastoma.BioData mining · 2025Article
- Research advances in epigenetic modifications and post-translational modifications in endothelial-mesenchymal transition.Epigenetics & chromatin · 2025Review
- The USP43/RNF2 axis negatively regulates antiviral innate immunity by promoting TBK1 ubiquitination and degradation.Cell death and differentiation · 2025Article
- HROB Induces Lung Adenocarcinoma Progression via ZC3HC1-CCNB1 Axis Regulation and Cell Cycle Dysregulation.Cancer science · 2025Article
- Toosendanin promotes prostate cancer cell apoptosis, ferroptosis and M1 polarization via USP39-mediated PLK1 deubiquitination.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- USP39 promote post-translational modifiers to stimulate the progress of cancer.Discover oncology · 2025Review
- Exploring the cancerous nexus: the pivotal and diverse roles of USP39 in cancer development.Discover oncology · 2025Review
- USP39 at the crossroads of cancer immunity: regulating immune evasion and immunotherapy response through RNA splicing and ubiquitin signaling.Frontiers in immunology · 2025Review
- USP39: a key regulator in malignant tumor progression.Frontiers in oncology · 2025Review
- Disrupting USP39 deubiquitinase function impairs the survival and migration of multiple myeloma cells through ZEB1 degradation.Journal of experimental & clinical cancer research : CR · 2024Article
- USP39 regulates pyruvate handling in non-small cell lung cancer.Cell death discovery · 2024Article
- USP39-Mediated Non-Proteolytic Control of ETS2 Suppresses Nuclear Localization and Activity.Biomolecules · 2023Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe elevated Cyclin B1 expression contributes to various tumorigenesis and poor prognosis. Cyclin B1 expression could be regulated by ubiquitination and deubiquitination. However, the mechanism of how Cyclin B1 is deubiquitinated and its roles in human glioma remain unclear.
methodsCo-immunoprecipitation and other assays were performed to detect the interacting of Cyclin B1 and USP39. A series of in vitro and in vivo experiments were performed to investigate the effect of USP39 on the tumorigenicity of tumor cells.
resultsUSP39 interacts with Cyclin B1 and stabilizes its expression by deubiquitinating Cyclin B1. Notably, USP39 cleaves the K29-linked polyubiquitin chain on Cyclin B1 at Lys242. Additionally, overexpression of Cyclin B1 rescues the arrested cell cycle at G2/M transition and the suppressed proliferation of glioma cells caused by USP39 knockdown in vitro. Furthermore, USP39 promotes the growth of glioma xenograft in subcutaneous and in situ of nude mice. Finally, in human tumor specimens, the expression levels of USP39 and Cyclin B1 are positively relevant.
conclusionOur data support the evidence that USP39 acts a novel deubiquitinating enzyme of Cyclin B1 and promoted tumor cell proliferation at least in part through Cyclin B1 stabilization, represents a promising therapeutic strategy for tumor patients.
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