ArticleNature communications2023
Metabolism-based targeting of MYC via MPC-SOD2 axis-mediated oxidation promotes cellular differentiation in group 3 medulloblastoma.
Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 16 citations in OpenAlex.
- Targeting SRC enhances differentiation and promotes multifaceted cell death mechanisms in recurrent group 3 medulloblastoma.Cell death & disease · 2026Article
- LncRNA-HLX-2-7/HLX axis-dependent metabolic reprogramming drives cancer progression in group 3 medulloblastoma.Acta neuropathologica communications · 2026Article
- Multiomic integration reveals tumoral heterogeneity of lipid dependence within lethal group 3 medulloblastoma.Cancer cell · 2026Article
- Medulloblastoma stem cell programs: Molecular roadmaps of disease progression.Developmental cell · 2026Review
- Targeting tumor metabolic flexibility enhances radiotherapeutic efficacy via mitochondrial complex I Inhibition in an intracranial S180 sarcoma mouse model.Scientific reports · 2025Article
- Deciphering Medulloblastoma: Epigenetic and Metabolic Changes Driving Tumorigenesis and Treatment Outcomes.Biomedicines · 2025Review
- Disease stage-specific role of the mitochondrial pyruvate carrier suppresses differentiation in temozolomide and radiation-treated glioblastoma.Neuro-oncology · 2025Article
- Article
- Mechanisms of metabolism-coupled protein modifications.Nature chemical biology · 2025Review
- Exploring Mechanisms and Biomarkers of Breast Cancer Invasion and Migration: An Explainable Gene-Pathway-Compounds Neural Network.Cancer medicine · 2025Article
- Article
- Targeting Group 3 Medulloblastoma by the Anti-PRUNE-1 and Anti-LSD1/KDM1A Epigenetic Molecules.International journal of molecular sciences · 2024Article
- Complex II ambiguities-FADHThe Journal of biological chemistry · 2024Review
Corrections and comments
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Authors and funding
14 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Group 3 medulloblastoma (G3 MB) carries the worst prognosis of all MB subgroups. MYC oncoprotein is elevated in G3 MB tumors; however, the mechanisms that support MYC abundance remain unclear. Using metabolic and mechanistic profiling, we pinpoint a role for mitochondrial metabolism in regulating MYC. Complex-I inhibition decreases MYC abundance in G3 MB, attenuates the expression of MYC-downstream targets, induces differentiation, and prolongs male animal survival. Mechanistically, complex-I inhibition increases inactivating acetylation of antioxidant enzyme SOD2 at K68 and K122, triggering the accumulation of mitochondrial reactive oxygen species that promotes MYC oxidation and degradation in a mitochondrial pyruvate carrier (MPC)-dependent manner. MPC inhibition blocks the acetylation of SOD2 and oxidation of MYC, restoring MYC abundance and self-renewal capacity in G3 MB cells following complex-I inhibition. Identification of this MPC-SOD2 signaling axis reveals a role for metabolism in regulating MYC protein abundance that has clinical implications for treating G3 MB.
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