ArticleCell death & disease2018
MYCN drives glutaminolysis in neuroblastoma and confers sensitivity to an ROS augmenting agent.
Article in Cell death & disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 70 citations in OpenAlex.
- MYCN-driven metabolic remodelling of the tumour microenvironment in neuroblastoma: implications for stromal biology and CAF heterogeneity.Cancer metastasis reviews · 2026Review
- Metabolic permissiveness: how tissue context shapes cancer.Genes & development · 2026Review
- 7,7"-dimethoxyagastisflavone induced MYCN/MYBL2-dependent apoptosis and metabolism reprogramming in Sonic Hedgehog medulloblastoma.Journal of translational medicine · 2026Article
- Cancer stem cell programs S-nitrosylation and deubiquitination of FoxP3 protein to promote regulatory T cell differentiation.Frontiers in immunology · 2026Article
- Dietary Polyphenol Combinations Have a Multifaceted Inhibitory Effect on Metabolic Rewiring and Signaling Pathways in Neuroblastoma.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Deciphering Medulloblastoma: Epigenetic and Metabolic Changes Driving Tumorigenesis and Treatment Outcomes.Biomedicines · 2025Review
- Inhibition of Purine Metabolism Promotes the Differentiation of Neuroblastoma Driven by MYCN.Cancer medicine · 2025Article
- Emerging Trends in Neuroblastoma Diagnosis, Therapeutics, and Research.Molecular neurobiology · 2025Review
- Oxphos targeting ofFrontiers in oncology · 2025Article
- Repurposing dimethyl fumarate for cancer therapy: current evidence and future directions.Frontiers in pharmacology · 2025Review
- Spliceosomal vulnerability of MYCN-amplified neuroblastoma is contingent on PRMT5-mediated regulation of epitranscriptomic and metabolomic pathways.Cancer letters · 2024Article
- L-Glyceraldehyde Inhibits Neuroblastoma Cell Growth via a Multi-Modal Mechanism on Metabolism and Signaling.Cancers · 2024Article
- Article
- Research progress in mechanism of anticancer action of shikonin targeting reactive oxygen species.Frontiers in pharmacology · 2024Review
- Mutational topography reflects clinical neuroblastoma heterogeneity.Cell genomics · 2023Article
- Triple Therapy with Metformin, Ketogenic Diet, and Metronomic Cyclophosphamide Reduced Tumor Growth in MYCN-Amplified Neuroblastoma Xenografts.Metabolites · 2023Article
- Clonal evolution during metastatic spread in high-risk neuroblastoma.Nature genetics · 2023Article
- Regulative Roles of Metabolic Plasticity Caused by Mitochondrial Oxidative Phosphorylation and Glycolysis on the Initiation and Progression of Tumorigenesis.International journal of molecular sciences · 2023Review
- Glutamine Metabolism in Cancer Stem Cells: A Complex Liaison in the Tumor Microenvironment.International journal of molecular sciences · 2023Review
- ONC201 Suppresses Neuroblastoma Growth by Interrupting Mitochondrial Function and Reactivating Nuclear ATRX Expression While Decreasing MYCN.International journal of molecular sciences · 2023Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Heightened aerobic glycolysis and glutaminolysis are characteristic metabolic phenotypes in cancer cells. Neuroblastoma (NBL), a devastating pediatric cancer, is featured by frequent genomic amplification of MYCN, a member of the Myc oncogene family that is primarily expressed in the early stage of embryonic development and required for neural crest development. Here we report that an enriched glutaminolysis gene signature is associated with MYCN amplification in children with NBL. The partial knockdown of MYCN suppresses glutaminolysis in NBL cells. Conversely, forced overexpression of MYCN in neural crest progenitor cells enhances glutaminolysis. Importantly, glutaminolysis induces oxidative stress by producing reactive oxygen species (ROS), rendering NBL cells sensitive to ROS augmentation. Through a small-scale metabolic-modulator screening, we have found that dimethyl fumarate (DMF), a Food and Drug Administration-approved drug for multiple sclerosis, suppresses NBL cell proliferation in vitro and tumor growth in vivo. DMF suppresses NBL cell proliferation through inducing ROS and subsequently suppressing MYCN expression, which is rescued by an ROS scavenger. Our findings suggest that the metabolic modulation and ROS augmentation could be used as novel strategies in treating NBL and other MYC-driven cancers.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.