ArticleScientific reports2020
N-Myc-induced metabolic rewiring creates novel therapeutic vulnerabilities in neuroblastoma.
Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 36 citations in OpenAlex.
- Targeting Cystine Addiction Suppresses Breast Cancer Lung Metastasis.Cancer research · 2026Article
- MYCN inhibits TrkC-mediated differentiation in neuroblastoma cells via disruption of the PKA signalling pathway.Cell death discovery · 2026Article
- Dietary Polyphenol Combinations Have a Multifaceted Inhibitory Effect on Metabolic Rewiring and Signaling Pathways in Neuroblastoma.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Review
- A computational model elucidates the effects of oncogene-induced expression alterations on the energy metabolism of neuroblastoma.Scientific reports · 2025Article
- Targeting Pathways in Neuroblastoma: Advances in Treatment Strategies and Clinical Outcomes.International journal of molecular sciences · 2025Review
- Molecular regulation and therapeutic targeting ofFrontiers in cell and developmental biology · 2025Review
- Defining neuroblastoma: From origin to precision medicine.Neuro-oncology · 2024Review
- Spliceosomal vulnerability of MYCN-amplified neuroblastoma is contingent on PRMT5-mediated regulation of epitranscriptomic and metabolomic pathways.Cancer letters · 2024Article
- A temporal (phospho-)proteomic dataset of neurotrophic receptor tyrosine kinase signalling in neuroblastoma.Scientific data · 2024Article
- Joint metabolomics and transcriptomics analysis systematically reveal the impact of MYCN in neuroblastoma.Scientific reports · 2024Article
- A Multi-Omics Approach Reveals Enrichment in Metabolites Involved in the Regulation of the Glutathione Pathway in LIN28B-Dependent Cancer Cells.International journal of molecular sciences · 2024Article
- Triple Therapy with Metformin, Ketogenic Diet, and Metronomic Cyclophosphamide Reduced Tumor Growth in MYCN-Amplified Neuroblastoma Xenografts.Metabolites · 2023Article
- Defining the landscape of circular RNAs in neuroblastoma unveils a global suppressive function of MYCN.Nature communications · 2023Article
- MYCL promotes the progression of triple‑negative breast cancer by activating the JAK/STAT3 pathway.Oncology reports · 2022Article
- MYCN and Metabolic Reprogramming in Neuroblastoma.Cancers · 2022Review
- A 3D Bioprinted in vitro Model of Neuroblastoma Recapitulates Dynamic Tumor-Endothelial Cell Interactions Contributing to Solid Tumor Aggressive Behavior.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022Article
- Prognostic analysis of E2F transcription factors E2F1 and E2F3 in four independent pediatric neuroblastoma cohorts.BMC pediatrics · 2022Article
- EIF4EBP1 is transcriptionally upregulated by MYCN and associates with poor prognosis in neuroblastoma.Cell death discovery · 2022Article
- Induced cell-autonomous neutropenia systemically perturbs hematopoiesis in Cebpa enhancer-null mice.Blood advances · 2022Article
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Authors and funding
14 authors at 6 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
N-Myc is a transcription factor that is aberrantly expressed in many tumor types and is often correlated with poor patient prognosis. Recently, several lines of evidence pointed to the fact that oncogenic activation of Myc family proteins is concomitant with reprogramming of tumor cells to cope with an enhanced need for metabolites during cell growth. These adaptions are driven by the ability of Myc proteins to act as transcriptional amplifiers in a tissue-of-origin specific manner. Here, we describe the effects of N-Myc overexpression on metabolic reprogramming in neuroblastoma cells. Ectopic expression of N-Myc induced a glycolytic switch that was concomitant with enhanced sensitivity towards 2-deoxyglucose, an inhibitor of glycolysis. Moreover, global metabolic profiling revealed extensive alterations in the cellular metabolome resulting from overexpression of N-Myc. Limited supply with either of the two main carbon sources, glucose or glutamine, resulted in distinct shifts in steady-state metabolite levels and significant changes in glutathione metabolism. Interestingly, interference with glutamine-glutamate conversion preferentially blocked proliferation of N-Myc overexpressing cells, when glutamine levels were reduced. Thus, our study uncovered N-Myc induction and nutrient levels as important metabolic master switches in neuroblastoma cells and identified critical nodes that restrict tumor cell proliferation.
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