ArticleInternational journal of radiation biology2019
Glutaminase inhibitor CB-839 increases radiation sensitivity of lung tumor cells and human lung tumor xenografts in mice.
Article in International journal of radiation biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers.
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Who cites it
74 citing papers in PubMed, 106 citations in OpenAlex.
- The role of glutamine metabolism in the pathogenesis of idiopathic pulmonary fibrosis and its therapeutic potential.Frontiers in oncology · 2026Review
- Advances in Metabolic Reprogramming and Immune Regulatory Mechanisms in Lung Cancer.Oncology research · 2026Review
- The Interdependence of Carbon Substrates and Metabolic Pathways Enables the Metabolic Plasticity of Cancer Cells.Advances in experimental medicine and biology · 2026Review
- Targeting Lung Cancer Metabolism: Therapeutic Opportunities and Challenges.Advances in experimental medicine and biology · 2026Review
- A pancancer analysis reveals the oncogenic role of glutaminase 1 (GLS1) in tumor metabolism and immune evasion: a bioinformatics analysis.Discover oncology · 2025Article
- Cell Death, Molecular Targeted Therapies, and Metabolic Reprogramming in EGFR-Mutant Lung Cancer.Cancers · 2025Review
- Disruption of glutamine transport uncouples the NUPR1 stress-adaptation program and induces prostate cancer radiosensitivity.Cell communication and signaling : CCS · 2025Article
- Unraveling the nexus: Genomic instability and metabolism in cancer.Cell reports · 2025Review
- Identification of immune characteristic biomarkers and therapeutic targets in cuproptosis for rheumatoid arthritis by integrated bioinformatics analysis and single-cell RNA sequencing analysis.Frontiers in medicine · 2025Article
- Metabolic reprogramming and therapeutic targeting in non-small cell lung cancer: emerging insights beyond the Warburg effect.Frontiers in oncology · 2025Review
- Fuel for thought: targeting metabolism in lung cancer.Translational lung cancer research · 2024Review
- Genomic predictors of radiation response: recent progress towards personalized radiotherapy for brain metastases.Cell death discovery · 2024Review
- CB-839 induces reversible dormancy in lung tumor-cells.European journal of pharmacology · 2024Article
- Cancer cell metabolism and antitumour immunity.Nature reviews. Immunology · 2024Review
- Glutamine and leukemia research: progress and clinical prospects.Discover oncology · 2024Review
- Glutamine Metabolism and Prostate Cancer.Cancers · 2024Review
- Unrestricted molecular motions enable mild photothermy for recurrence-resistant FLASH antitumor radiotherapy.Bioactive materials · 2024Article
- Metabolic Reprogramming in Thyroid Cancer.Endocrinology and metabolism (Seoul, Korea) · 2024Review
- Acquired Radiation Resistance Induces Thiol-dependent Cisplatin Cross-resistance.Radiation research · 2024Article
- Molecular mechanism of glutaminase activation through filamentation and the role of filaments in mitophagy protection.Nature structural & molecular biology · 2023Article
14 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
purposeThe purpose of this study was to translate our in vitro therapy approach to an in vivo model. Increased glutamine uptake is known to drive cancer cell proliferation, making tumor cells glutamine-dependent. Studying lymph-node aspirates containing malignant lung tumor cells showed a strong correlation between glutamine consumption and glutathione (GSH) excretion. Subsequent experiments with A549 and H460 lung tumor cell lines provided additional evidence for glutamine's role in driving synthesis and excretion of GSH. Using stable-isotope-labeled glutamine as a tracer metabolite, we demonstrated that the glutamate group in GSH is directly derived from glutamine, linking glutamine utilization intimately to GSH syntheses. MATERIALS AND
methodsTo understand the possible mechanistic link between glutamine consumption and GSH excretion, we studied GSH metabolism in more detail. Inhibition of glutaminase (GLS) with BPTES, a GLS-specific inhibitor, effectively abolished GSH synthesis and excretion. Since our previous work, several novel GLS inhibitors became available and we report herein effects of CB-839 in A427, H460 and A549 lung tumor cells and human lungtumor xenografts in mice.
resultsInhibition of GLS markedly reduced cell viability, producing ED
conclusionThe results support the proposed mechanistic link between GLS activity and GSH synthesis and suggest that GLS inhibitors are effective radiosensitizers.
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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.