ArticleScientific reports2017
Metabolic Differences in Glutamine Utilization Lead to Metabolic Vulnerabilities in Prostate Cancer.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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.
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Who cites it
44 citing papers in PubMed, 68 citations in OpenAlex.
- MR-based techniques for imaging prostate cancer metabolism: current status and future perspectives.Abdominal radiology (New York) · 2026Review
- Simvastatin reprograms lipid metabolism in B16.F10 melanoma cells to favor an early resistant phenotype.Scientific reports · 2026Article
- Fueling Prostate Cancer: The Central Role of Glutamine/Glutamate Metabolic Reprogramming.Asian Pacific journal of cancer prevention : APJCP · 2025Review
- Targeting Prostate Cancer Metabolism Through Transcriptional and Epigenetic Modulation: A Multi-Target Approach to Therapeutic Innovation.International journal of molecular sciences · 2025Review
- Combination of Low-Dose Sulforaphane and Docetaxel on Mitochondrial Function and Metabolic Reprogramming in Prostate Cancer Cell Lines.International journal of molecular sciences · 2025Article
- Intrinsic apoptotic effect of Anatolian honeybee (Turkish journal of biology = Turk biyoloji dergisi · 2025Article
- Article
- The causal effect of serum amino acids on the risk of prostate cancer: a two-sample mendelian randomization study.Scientific reports · 2024Article
- The Anti-proliferative Effect of a Novel Glutaminase Inhibitor IN-3 on Prostate Cancer Cells.Medeniyet medical journal · 2024Article
- Glutamine Metabolism and Prostate Cancer.Cancers · 2024Review
- Targeting the glutamine metabolism to suppress cell proliferation in mesenchymal docetaxel-resistant prostate cancer.Oncogene · 2024Article
- METTL14 downregulation drives S100A4Signal transduction and targeted therapy · 2024Article
- Molecular mechanism of glutaminase activation through filamentation and the role of filaments in mitophagy protection.Nature structural & molecular biology · 2023Article
- Metabolic Alterations in Canine Mammary Tumors.Animals : an open access journal from MDPI · 2023Review
- Article
- Reflections on the Biology of Cell Culture Models: Living on the Edge of Oxidative Metabolism in Cancer Cells.International journal of molecular sciences · 2023Review
- Targeting Glutamine Metabolism in Prostate Cancer.Frontiers in bioscience (Elite edition) · 2023Review
- Novel insight into metabolic reprogrammming in cancer radioresistance: A promising therapeutic target in radiotherapy.International journal of biological sciences · 2023Review
- Druggable Metabolic Vulnerabilities Are Exposed and Masked during Progression to Castration Resistant Prostate Cancer.Biomolecules · 2022Review
- Dual contribution of the mTOR pathway and of the metabolism of amino acids in prostate cancer.Cellular oncology (Dordrecht, Netherlands) · 2022Review
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
Abstract
The new oncologic paradigm of precision medicine is focused on identifying metabolic, proteomic, transcriptomic and genomic variabilities in tumors that can be exploited to tailor treatments and improve patient outcomes. Metabolic changes are a hallmark of cancer, and inhibition of metabolic pathways is now a major strategy in medicinal chemistry for targeting cancers. However, non-invasive biomarkers to categorize metabolic subtypes are in short supply. The purpose of this study was to characterize the intracellular and extracellular metabolic profiles of four prostate cancer cell lines with varying degrees of aggressiveness. We observed metabolic differences between the aggressive prostate cancer cell line PC3 and the even more aggressive, metastatic subline PC3M assessed by hyperpolarized in vivo pyruvate studies, nuclear magnetic resonance spectroscopy, and carbon-13 feeding studies. On further examination of the differences between these two cell lines, we found increased glutamine utilization in the metastatic PC3M subline that led directly to sensitivity to glutaminase inhibitor CB-839. Our study supports the theory that metastatic progression increases glutamine utilization and the inhibition of glutaminolysis could have clinical implications.
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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.