ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025
HDAC6 and USP9X Control Glutamine Metabolism by Stabilizing GS to Promote Glioblastoma Tumorigenesis.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
6 citing papers in PubMed.
- The histone deacetylase family in health and disease.Signal transduction and targeted therapy · 2026Review
- Histone deacetylases in cancer metabolic reprogramming.Experimental & molecular medicine · 2026Review
- Metabolic remodeling by circular RNAs in gastric tumorigenesis: From mechanisms to biomarker discovery (Review).International journal of oncology · 2026Review
- Targeting tumor dormancy: the next frontier in gastrointestinal stromal tumor therapy.Neoplasia (New York, N.Y.) · 2026Review
- USP10 deubiquitinase: Physiological function, diseases and therapeutic target (Review).International journal of molecular medicine · 2026Review
- HDAC6 and USP9X Control Glutamine Metabolism by Stabilizing GS to Promote Glioblastoma Tumorigenesis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
Glioblastoma (GBM) is the most common and the deadliest brain cancer. Glutamine anabolism mediated by glutamine synthetase (GS) is beneficial for GBM cell growth, especially under glutamine deprivation. However, the molecular mechanism underlying GS homeostasis in GBM remains undisclosed. Here, it is reported that histone deacetylase 6 (HDAC6) promotes GS deacetylation, stabilizing it via ubiquitin-mediated pathway. It is found that deubiquitination of GS is modulated by ubiquitin-specific peptidase 9, X-linked (USP9X). USP9X stabilizes GS by removing its K48-linked polyubiquitination on lysine 91 and 103. Accordingly, targeting HDAC6 and USP9X in vitro and in vivo represses GBM tumorigenesis by decreasing GS stability. Metabolic analysis shows that silencing HDAC6 and USP9X disrupts de novo nucleotide synthesis, thereby attenuating GBM cell growth. Furthermore, GS modulation by targeting HDAC6 and USP9X restrains the self-renewal capacity. These results suggest that HDAC6 and USP9X are crucial epigenetic enzymes that promote GBM tumorigenesis by modulating glutamine metabolism.
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