ArticlePloS one2014
Rapid analysis of glycolytic and oxidative substrate flux of cancer cells in a microplate.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 95 papers.
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Who cites it
95 citing papers in PubMed.
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- Palmitic acid induces UCP1-independent mitochondrial depolarization specifically in brown adipose tissue.The Journal of biological chemistry · 2026Article
- Early metabolic reprogramming and carbonic anhydrase IX-mediated extracellular acidification drive radiotherapy-induced glioblastoma cell dedifferentiation.Acta neuropathologica communications · 2025Article
- Effects of anserine on oxidative stress and on cell barrier integrity in methylmalonic aciduria.Scientific reports · 2025Article
- Non-canonical nuclear function of glutaminase cooperates with Wnt signaling to drive EMT during neural crest development.Nature communications · 2025Article
- BCR::ABL1 expression in chronic myeloid leukemia cells in low oxygen is regulated by glutamine via CD36-mediated fatty acid uptake.Cancer cell international · 2025Article
- Proinflammatory Cytokines Enhance the Mineralization, Proliferation, and Metabolic Activity of Primary Human Osteoblast-like Cells.International journal of molecular sciences · 2024Article
- Aquaporins in colorectal cancer: exploring their role in tumorigenesis, metastasis, and drug response.Human cell · 2024Review
- Cerium Oxide Nanozymes Improve Skeletal Muscle Function in Gestational Diabetic Offspring by Attenuating Mitochondrial Oxidative Stress.ACS omega · 2024Article
- Chaga mushroom extract suppresses oral cancer cell growth via inhibition of energy metabolism.Scientific reports · 2024Article
- Kinetic modelling of the cellular metabolic responses underpinning in vitro glycolysis assays.FEBS open bio · 2024Article
- Neuron-astrocyte metabolic coupling facilitates spinal plasticity and maintenance of inflammatory pain.Nature metabolism · 2024Article
- 9-HODE and 9-HOTrE alter mitochondrial metabolism, increase triglycerides, and perturb fatty acid uptake and synthesis associated gene expression in HepG2 cells.Prostaglandins, leukotrienes, and essential fatty acids · 2024Article
- Novel Pan-ERR Agonists Ameliorate Heart Failure Through Enhancing Cardiac Fatty Acid Metabolism and Mitochondrial Function.Circulation · 2024Article
- Effect ofInternational journal of molecular sciences · 2023Article
- Standardized In Vitro Models of Human Adipose Tissue Reveal Metabolic Flexibility in Brown Adipocyte Thermogenesis.Endocrinology · 2023Article
- Article
- Osteoarthritic chondrocytes undergo a glycolysis-related metabolic switch upon exposure to IL-1b or TNF.Cell communication and signaling : CCS · 2023Article
35 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cancer cells exhibit remarkable alterations in cellular metabolism, particularly in their nutrient substrate preference. We have devised several experimental methods that rapidly analyze the metabolic substrate flux in cancer cells: glycolysis and the oxidation of major fuel substrates glucose, glutamine, and fatty acids. Using the XF Extracellular Flux analyzer, these methods measure, in real-time, the oxygen consumption rate (OCR) and extracellular acidification rate (ECAR) of living cells in a microplate as they respond to substrates and metabolic perturbation agents. In proof-of-principle experiments, we analyzed substrate flux and mitochondrial bioenergetics of two human glioblastoma cell lines, SF188s and SF188f, which were derived from the same parental cell line but proliferate at slow and fast rates, respectively. These analyses led to three interesting observations: 1) both cell lines respired effectively with substantial endogenous substrate respiration; 2) SF188f cells underwent a significant shift from glycolytic to oxidative metabolism, along with a high rate of glutamine oxidation relative to SF188s cells; and 3) the mitochondrial proton leak-linked respiration of SF188f cells increased significantly compared to SF188s cells. It is plausible that the proton leak of SF188f cells may play a role in allowing continuous glutamine-fueled anaplerotic TCA cycle flux by partially uncoupling the TCA cycle from oxidative phosphorylation. Taken together, these rapid, sensitive and high-throughput substrate flux analysis methods introduce highly valuable approaches for developing a greater understanding of genetic and epigenetic pathways that regulate cellular metabolism, and the development of therapies that target cancer metabolism.
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