ArticleNeuro-oncology2017
The angiogenic switch leads to a metabolic shift in human glioblastoma.
Article in Neuro-oncology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
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Who cites it
56 citing papers in PubMed, 75 citations in OpenAlex.
- Mitochondria transfer in glioblastoma.Neuro-oncology · 2026Review
- AATF supports proliferation of glioblastoma cells by sustaining mitochondrial respiration through an NRF-1-dependent mechanism.Cell death & disease · 2026Article
- Absolute dynamic and relative static: the relationship of glycolysis and OXPHOS in cancer development.Cell death discovery · 2026Review
- Targeting Metabolic Vulnerabilities in Glioblastoma: a Framework for Multi-node Combination Therapy.Current oncology reports · 2026Review
- CMROLa Radiologia medica · 2025Article
- Semaphorin 6A phase separation sustains a histone lactylation-dependent lactate buildup in pathological angiogenesis.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Glutaminolysis is associated with mitochondrial pathway activation and can be therapeutically targeted in glioblastoma.Cancer & metabolism · 2024Article
- BMP4 and Temozolomide Synergize in the Majority of Patient-Derived Glioblastoma Cultures.International journal of molecular sciences · 2024Article
- Predicting intercellular communication based on metabolite-related ligand-receptor interactions with MRCLinkdb.BMC biology · 2024Article
- Review
- Blood-Brain Barrier-Targeting Nanoparticles: Biomaterial Properties and Biomedical Applications in Translational Neuroscience.Pharmaceuticals (Basel, Switzerland) · 2024Review
- New Insights in ATP Synthesis as Therapeutic Target in Cancer and Angiogenic Ocular Diseases.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2024Review
- MACC: a visual interactive knowledgebase of metabolite-associated cell communications.Nucleic acids research · 2024Article
- Role of UBE2C in Brain Cancer Invasion and Dissemination.International journal of molecular sciences · 2023Review
- The Inhibition of the FGFR/PI3K/Akt Axis by AZD4547 Disrupts the Proangiogenic Microenvironment and Vasculogenic Mimicry Arising from the Interplay between Endothelial and Triple-Negative Breast Cancer Cells.International journal of molecular sciences · 2023Article
- Targeting tumor microenvironment using tumor-infiltrating lymphocytes as therapeutics against tumorigenesis.Immunologic research · 2023Review
- GAP43-dependent mitochondria transfer from astrocytes enhances glioblastoma tumorigenicity.Nature cancer · 2023Article
- Interactions between microglia and glioma in tumor microenvironment.Frontiers in oncology · 2023Review
- Tumor-secreted lactate contributes to an immunosuppressive microenvironment and affects CD8 T-cell infiltration in glioblastoma.Frontiers in immunology · 2023Article
- Lactate dehydrogenases promote glioblastoma growth and invasion via a metabolic symbiosis.EMBO molecular medicine · 2022Article
Corrections and comments
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Authors and funding
21 authors at 6 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Invasion and angiogenesis are major hallmarks of glioblastoma (GBM) growth. While invasive tumor cells grow adjacent to blood vessels in normal brain tissue, tumor cells within neovascularized regions exhibit hypoxic stress and promote angiogenesis. The distinct microenvironments likely differentially affect metabolic processes within the tumor cells. Methods: In the present study, we analyzed gene expression and metabolic changes in a human GBM xenograft model that displayed invasive and angiogenic phenotypes. In addition, we used glioma patient biopsies to confirm the results from the xenograft model. Results: We demonstrate that the angiogenic switch in our xenograft model is linked to a proneural-to-mesenchymal transition that is associated with upregulation of the transcription factors BHLHE40, CEBPB, and STAT3. Metabolic analyses revealed that angiogenic xenografts employed higher rates of glycolysis compared with invasive xenografts. Likewise, patient biopsies exhibited higher expression of the glycolytic enzyme lactate dehydrogenase A and glucose transporter 1 in hypoxic areas compared with the invasive edge and lower-grade tumors. Analysis of the mitochondrial respiratory chain showed reduction of complex I in angiogenic xenografts and hypoxic regions of GBM samples compared with invasive xenografts, nonhypoxic GBM regions, and lower-grade tumors. In vitro hypoxia experiments additionally revealed metabolic adaptation of invasive tumor cells, which increased lactate production under long-term hypoxia. Conclusions: The use of glycolysis versus mitochondrial respiration for energy production within human GBM tumors is highly dependent on the specific microenvironment. The metabolic adaptability of GBM cells highlights the difficulty of targeting one specific metabolic pathway for effective therapeutic intervention.
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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.