ArticleCell death discovery2021
ADO/hypotaurine: a novel metabolic pathway contributing to glioblastoma development.
Article in Cell death discovery, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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The trial behind it
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Who cites it
19 citing papers in PubMed.
- Causal Associations of Cerebrospinal Fluid and Circulating Metabolites With Malignant Brain Neoplasms: A Mendelian Randomization Analysis.Brain and behavior · 2026Article
- The Role of the Cysteamine Dioxygenase (ADO) Gene in Atopic Dermatitis.Acta dermato-venereologica · 2026Article
- Proteomic profiling reveals dynamic regulation of vesicle trafficking across glioma grades.Journal of neuro-oncology · 2025Article
- Hydralazine inhibits cysteamine dioxygenase to treat preeclampsia and senesce glioblastoma.Science advances · 2025Article
- The emerging intertwined activities of metabolism and epigenetics unveils culprits and prospects in cancer.Experimental & molecular medicine · 2025Review
- Human adenovirus serotype 5 infection dysregulates cysteine, purine, and unsaturated fatty acid metabolism in fibroblasts.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Taurine Synthesis by 2-Aminoethanethiol Dioxygenase as a Vulnerable Metabolic Alteration in Pancreatic Cancer.Biomolecules & therapeutics · 2025Article
- Hydralazine inhibits cysteamine dioxygenase to treat preeclampsia and senesce glioblastoma.bioRxiv : the preprint server for biology · 2024Article
- Cysteamine dioxygenase (ADO) governs cancer cell mitochondrial redox homeostasis through proline metabolism.Science advances · 2024Article
- The role of cytidine 5'-triphosphate synthetase 1 in metabolic rewiring during epithelial-to-mesenchymal transition in non-small-cell lung cancer.FEBS open bio · 2024Article
- ABLIM1, a novel ubiquitin E3 ligase, promotes growth and metastasis of colorectal cancer through targeting IĸBα ubiquitination and activating NF-ĸB signaling.Cell death and differentiation · 2024Article
- Dysregulated lipid metabolism in TMZ-resistant glioblastoma: pathways, proteins, metabolites and therapeutic opportunities.Lipids in health and disease · 2023Review
- The Recent Research Progress of NF-κB Signaling on the Proliferation, Migration, Invasion, Immune Escape and Drug Resistance of Glioblastoma.International journal of molecular sciences · 2023Review
- Rewired Metabolism of Amino Acids and Its Roles in Glioma Pathology.Metabolites · 2022Review
- The Crystal Structure of Cysteamine Dioxygenase Reveals the Origin of the Large Substrate Scope of This Vital Mammalian Enzyme.Biochemistry · 2021Article
- The role of metabolic ecosystem in cancer progression - metabolic plasticity and mTOR hyperactivity in tumor tissues.Cancer metastasis reviews · 2021Review
- Review
- Glucose and Amino Acid Metabolic Dependencies Linked to Stemness and Metastasis in Different Aggressive Cancer Types.Frontiers in pharmacology · 2021Review
- Metabolomic and lipidomic profiling reveals distinct subtypes of glioblastoma IDH-wildtype and shared metabolic features with astrocytoma IDH-mutant grade 4.Neuro-oncology advancesArticle
Corrections and comments
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Significant advance has been made towards understanding glioblastoma metabolism through global metabolomic profiling. However, hitherto little is known about the role by which altered metabolism plays in driving the aggressive glioma phenotype. We have previously identified hypotaurine as one of the top-ranked metabolites for differentiating low- and high-grade tumors, and that there is also a strong association between the levels of intratumoral hypotaurine and expression of its biosynthetic enzyme, cysteamine (2-aminoethanethiol) dioxygenase (ADO). Using transcription profiling, we further uncovered that the ADO/hypotaurine axis targets CCL20 secretion through activating the NF-κB pathway to drive the self-renewal and maintenance of glioma 'cancer stem cells' or glioma cancer stem-like cells. Conversely, abrogating the ADO/hypotaurine axis using CRISPR/Cas9-mediated gene editing limited glioblastoma cell proliferation and self-renewal in vitro and tumor growth in vivo in an orthotopical mouse model, indicating that this metabolic pathway is a potential key therapeutic target. Collectively, our results unveil a targetable metabolic pathway, which contributes to the growth and progression of aggressive high-grade gliomas, as well as a novel predictive marker for glioblastoma diagnosis and therapy.
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Registered trials
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