ArticleCancer research2017
MYC-Regulated Mevalonate Metabolism Maintains Brain Tumor-Initiating Cells.
Article in Cancer research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers, 2 of them syntheses that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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
80 citing papers in PubMed, 2 syntheses or guidelines pooled it, 116 citations in OpenAlex.
- Aberrant Energy Metabolism in Tumors and Potential Therapeutic Targets.Genes, chromosomes & cancer · 2024Pooled it
- Pooled it
- H2AX phosphorylation driven by the SET-PP2A axis maintains glioma stem cell properties.Genes & diseases · 2026Article
- Uric acid enhances tumor stemness in breast cancer cells by upregulating GMPS.Molecular medicine reports · 2026Article
- Overcoming Chemoresistance in Glioblastoma: Mechanisms, Therapeutic Strategies, and Functional Precision Medicine.International journal of molecular sciences · 2026Review
- OSBPL2-mediated lipid metabolism alteration governs lung cancer stem cells properties.Stem cell research & therapy · 2026Article
- Disrupting PDGFRA-driven immune evasion in glioma: vaccine-based strategies on the horizon.Frontiers in oncology · 2026Review
- Cholesterol metabolism in LUAD progression: GJB3 as a key target for cell‑based therapeutic interventions.Molecular medicine reports · 2025Article
- Cholesterol metabolism on stem cell fate determination: a frontier horizon.Stem cell research & therapy · 2025Review
- Cut the fat: targeting cholesterol and lipid metabolism in glioblastoma.Cell death & disease · 2025Review
- Nuclear cholesterol regulates nuclear size and DNA damage responses in cancer stem cells.Neuro-oncology · 2025Article
- Lipid metabolism: the potential therapeutic targets in glioblastoma.Cell death discovery · 2025Review
- NSDHL contributes to breast cancer stem-like cell maintenance and tumor-initiating capacity through TGF-β/Smad signaling pathway in MCF-7 tumor spheroid.BMC cancer · 2024Article
- Regulatory network analysis based on integrated miRNA-TF reveals key genes in heart failure.Scientific reports · 2024Article
- Targeting lipid reprogramming in the tumor microenvironment by traditional Chinese medicines as a potential cancer treatment.Heliyon · 2024Review
- Metabolic Roles of HIF1, c-Myc, and p53 in Glioma Cells.Metabolites · 2024Review
- OGDH and Bcl-xL loss causes synthetic lethality in glioblastoma.JCI insight · 2024Article
- The roles and molecular mechanisms of non-coding RNA in cancer metabolic reprogramming.Cancer cell international · 2024Review
- Lymphatic endothelial-like cells promote glioblastoma stem cell growth through cytokine-driven cholesterol metabolism.Nature cancer · 2024Article
- Review
20 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
21 authors at 2 institutions in 1 country.
Funding
Abstract
Metabolic dysregulation drives tumor initiation in a subset of glioblastomas harboring isocitrate dehydrogenase (IDH) mutations, but metabolic alterations in glioblastomas with wild-type IDH are poorly understood. MYC promotes metabolic reprogramming in cancer, but targeting MYC has proven notoriously challenging. Here, we link metabolic dysregulation in patient-derived brain tumor-initiating cells (BTIC) to a nexus between MYC and mevalonate signaling, which can be inhibited by statin or 6-fluoromevalonate treatment. BTICs preferentially express mevalonate pathway enzymes, which we find regulated by novel MYC-binding sites, validating an additional transcriptional activation role of MYC in cancer metabolism. Targeting mevalonate activity attenuated RAS-ERK-dependent BTIC growth and self-renewal. In turn, mevalonate created a positive feed-forward loop to activate MYC signaling via induction of miR-33b. Collectively, our results argue that MYC mediates its oncogenic effects in part by altering mevalonate metabolism in glioma cells, suggesting a therapeutic strategy in this setting.
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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.