ArticleCell death & disease2018
Metabolic reprogramming of acute lymphoblastic leukemia cells in response to glucocorticoid treatment.
Article in Cell death & disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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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
32 citing papers in PubMed, 48 citations in OpenAlex.
- Impact of lymphocyte p-glycoprotein activity on development of graft-versus-host disease after stem cell transplantation.International journal of hematology · 2026Article
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- Intestinal epithelial Ceacam1 deficiency prevents steroid-refractory acute gut graft-versus-host disease.JCI insight · 2025Article
- Metabolomic insights into pathogenesis and therapeutic potential in adult acute lymphoblastic leukemia.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Genome-wide study identifies novel genes associated with bone toxicities in children with acute lymphoblastic leukaemia.British journal of haematology · 2024Article
- Targeting autophagy as a therapeutic strategy in pediatric acute lymphoblastic leukemia.Scientific reports · 2024Article
- Klf9 plays a critical role in GR -dependent metabolic adaptations in cardiomyocytes.Cellular signalling · 2023Article
- 1,5-Anhydroglucitol promotes pre-B acute lymphocytic leukemia progression by driving glycolysis and reactive oxygen species formation.BMC cancer · 2023Article
- Dexamethasone-Induced Fatty Acid Oxidation and Autophagy/Mitophagy Are Essential for T-ALL Glucocorticoid Resistance.Cancers · 2023Article
- The glucocorticoid dexamethasone inhibits HIF-1α stabilization and metabolic reprogramming in lipopolysaccharide-stimulated primary macrophages.Discovery immunology · 2023Article
- Metabolic regulation of endothelial senescence.Frontiers in cardiovascular medicine · 2023Review
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- Urinary metabotype of severe asthma evidences decreased carnitine metabolism independent of oral corticosteroid treatment in the U-BIOPRED study.The European respiratory journal · 2022Article
- Steroid-Refractory Gut Graft-Versus-Host Disease: What We Have Learned From Basic Immunology and Experimental Mouse Model.Frontiers in immunology · 2022Review
- Deciphering Metabolic Adaptability of Leukemic Stem Cells.Frontiers in oncology · 2022Review
- Disrupted Alpha-Ketoglutarate Homeostasis: Understanding Kidney Diseases from the View of Metabolism and Beyond.Diabetes, metabolic syndrome and obesity : targets and therapy · 2022Review
- One Omics Approach Does Not Rule Them All: The Metabolome and the Epigenome Join Forces in Haematological Malignancies.Epigenomes · 2021Review
- Autophagy and Metabolism in Normal and Malignant Hematopoiesis.International journal of molecular sciences · 2021Review
- Metabolic reprogramming of inner ear cell line HEI-OC1 after dexamethasone application.Metabolomics : Official journal of the Metabolomic Society · 2021Article
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glucocorticoids (GCs) are metabolic hormones with immunosuppressive effects that have proven effective drugs against childhood acute lymphoblastic leukemia (ALL). Yet, the role of metabolic reprogramming in GC-induced ALL cell death is poorly understood. GCs efficiently block glucose uptake and metabolism in ALL cells, but this does not fully explain the observed induction of autophagy and cell death. Here, we have performed parallel time-course proteomics, metabolomics, and isotope-tracing studies to examine in detail the metabolic effects of GCs on ALL cells. We observed metabolic events associated with growth arrest, autophagy, and catabolism prior to onset of apoptosis: nucleotide de novo synthesis was reduced, while certain nucleobases accumulated; polyamine synthesis was inhibited; and phosphatidylcholine synthesis was induced. GCs suppressed not only glycolysis but also entry of both glucose and glutamine into the TCA cycle. In contrast, expression of glutamine-ammonia ligase (GLUL) and cellular glutamine content was robustly increased by GC treatment, suggesting induction of glutamine synthesis, similar to nutrient-starved muscle. Modulating medium glutamine and dimethyl-α-ketoglutarate (dm-αkg) to favor glutamine synthesis reduced autophagosome content of ALL cells, and dm-αkg also rescued cell viability. These data suggest that glutamine synthesis affects autophagy and possibly onset of cell death in response to GCs, which should be further explored to understand mechanism of action and possible sources of resistance.
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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.