ArticleClinical cancer research : an official journal of the American Association for Cancer Research2025
UBE2T-Mediated HP1α Ubiquitination Enhances Nucleolar Function and Promotes the Progression of IDH1/TP53-Mutant Glioma.
Article in Clinical cancer research : an official journal of the American Association for Cancer Research, 2025. 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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Who cites it
2 citing papers in PubMed.
- DDX5 (p68) and UbE2T as emerging superior cancer therapeutic targets: dual molecular glue target degradation by FL118 for conquering difficult-to-treat cancers.Journal of experimental & clinical cancer research : CR · 2026Review
- Ubiquitin-conjugating Enzymes in Cancer.International journal of biological sciences · 2026Review
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Authors and funding
9 authors.
Funding
Abstract
purposeHigh-grade glioma is the most aggressive form of primary brain tumor, characterized by rapid progression and a grim prognosis. The presence of mutations in IDH1 and TP53 is associated with a specific molecular phenotype in glioma, and their interaction is a potential target for therapy. EXPERIMENTAL
designOur study utilized a combination of bioinformatics analysis, in vitro experiments, and in vivo tumor xenograft models to investigate the role of the ubiquitin-conjugating enzyme 2T (UBE2T) in the malignant progression of IDH1/TP53-mutant glioma.
resultsWe found that UBE2T is overexpressed in the context of TP53 mutations and is linked to enhanced glioma cell proliferation and stemness. Mechanistically, UBE2T was shown to degrade HP1α via the ubiquitin-proteasome pathway, leading to the release of the suppressive effects of R-2-hydroxyglutarate on nucleolar function and an increase in rDNA transcription. The therapeutic potential of targeting UBE2T is underscored by the discovery that APR-246, a mutant p53 reactivator, effectively suppresses UBE2T expression and reverses the hyperactivity of nucleolar transcription.
conclusionsThese findings suggest that UBE2T plays a crucial role in the progression of IDH1/TP53-mutant astrocytoma and that targeting UBE2T with APR-246 could be a promising therapeutic strategy for patients with these mutations. Our study provides a foundation for further research into the role of UBE2T in glioma and the development of targeted therapies.
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