ArticleJournal of proteome research2017
Glucose Limitation Alters Glutamine Metabolism in MUC1-Overexpressing Pancreatic Cancer Cells.
Article in Journal of proteome research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 35 citations in OpenAlex.
- MUC1-EGFR crosstalk with IL-6 by activating NF-κB and MAPK pathways to regulate the stemness and paclitaxel-resistance of lung adenocarcinoma.Annals of medicine · 2024Article
- The Role of Lipid Metabolism Disorders in the Development of Thyroid Cancer.International journal of molecular sciences · 2024Review
- Mitochondrial enzyme FAHD1 reduces ROS in osteosarcoma.Scientific reports · 2024Article
- The MUC1-HIF-1α signaling axis regulates pancreatic cancer pathogenesis through polyamine metabolism remodeling.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Single-cell analysis reveals landscape of endometrial cancer response to estrogen and identification of early diagnostic markers.PloS one · 2024Article
- Advances in immunotherapy for triple-negative breast cancer.Molecular cancer · 2023Review
- The multifaceted role of MUC1 in tumor therapy resistance.Clinical and experimental medicine · 2023Review
- Deoxythymidylate kinase (DTYMK) participates in cell cycle arrest to promote pancreatic adenocarcinoma progression regulated by miR-491-5p through TP53 and is associated with tumor immune infiltration.Journal of gastrointestinal oncology · 2023Article
- Mitochondrial Metabolism in Pancreatic Ductal Adenocarcinoma: From Mechanism-Based Perspectives to Therapy.Cancers · 2023Review
- Metabolic Rewiring by Loss of Sirt5 Promotes Kras-Induced Pancreatic Cancer Progression.Gastroenterology · 2021Article
- MUC1: Structure, Function, and Clinic Application in Epithelial Cancers.International journal of molecular sciences · 2021Review
- Adaptation of pancreatic cancer cells to nutrient deprivation is reversible and requires glutamine synthetase stabilization by mTORC1.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- NAD-dependent methylenetetrahydrofolate dehydrogenase inhibits oral squamous cell carcinoma cell proliferation and promotes apoptosis.Translational cancer research · 2021Article
- Metabolic Reprogramming of Thyroid Cancer Cells and Crosstalk in Their Microenvironment.Frontiers in oncology · 2021Review
- Glucose and Amino Acid Metabolic Dependencies Linked to Stemness and Metastasis in Different Aggressive Cancer Types.Frontiers in pharmacology · 2021Review
- Review
- Targets (Metabolic Mediators) of Therapeutic Importance in Pancreatic Ductal Adenocarcinoma.International journal of molecular sciences · 2020Review
- Mucins in pancreatic cancer: A well-established but promising family for diagnosis, prognosis and therapy.Journal of cellular and molecular medicine · 2020Review
- MUC1 oncoprotein mitigates ER stress via CDA-mediated reprogramming of pyrimidine metabolism.Oncogene · 2020Article
- Beta 2-microglobulin regulates amyloid precursor-like protein 2 expression and the migration of pancreatic cancer cells.Cancer biology & therapy · 2019Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
Pancreatic cancer cells overexpressing Mucin 1 (MUC1) rely on aerobic glycolysis and, correspondingly, are dependent on glucose for survival. Our NMR metabolomics comparative analysis of control (S2-013.Neo) and MUC1-overexpressing (S2-013.MUC1) cells demonstrates that MUC1 reprograms glutamine metabolism upon glucose limitation. The observed alteration in glutamine metabolism under glucose limitation was accompanied by a relative decrease in the proliferation of MUC1-overexpressing cells compared with steady-state conditions. Moreover, glucose limitation induces G1 phase arrest where S2-013.MUC1 cells fail to enter S phase and synthesize DNA because of a significant disruption in pyrimidine nucleotide biosynthesis. Our metabolomics analysis indicates that glutamine is the major source of oxaloacetate in S2-013.Neo and S2-013.MUC1 cells, where oxaloacetate is converted to aspartate, an important metabolite for pyrimidine nucleotide biosynthesis. However, glucose limitation impedes the flow of glutamine carbons into the pyrimidine nucleotide rings and instead leads to a significant accumulation of glutamine-derived aspartate in S2-013.MUC1 cells.
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Registered trials
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