ArticleScience advances2021
Oxidative phosphorylation enhances the leukemogenic capacity and resistance to chemotherapy of B cell acute lymphoblastic leukemia.
Article in Science advances, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 76 citations in OpenAlex.
- CREB1 and GSK3 Isoforms as Potential Adaptive Signaling Nodes in PI3K/Akt/mTOR Inhibitor Treated Philadelphia Chromosome-Positive B-ALL.International journal of molecular sciences · 2026Article
- Elesclomol-mediated cuproptosis overcomes cisplatin resistance by restricting epigenetically activated mitochondrial respiration: Novel therapeutic insights into cisplatin-elesclomol combination therapy.Acta pharmaceutica Sinica. B · 2026Article
- An integrative molecular map of pediatric B-cell precursor acute lymphoblastic leukemia.Communications medicine · 2026Article
- Mitochondrial DNA mutations and intercellular mitochondrial transfer in cancer: mechanisms, biological effects, and clinical potential.Biomarker research · 2026Review
- Mechanistic role of glycolytic pathways in the tumor microenvironment in driving chemoresistance.Frontiers in cell and developmental biology · 2026Review
- The S-depalmitoylase ABHD10 is essential for sperm mitochondrial sheath formation and male fertility.Nature communications · 2025Article
- Immunometabolic Dysregulation in B-Cell Acute Lymphoblastic Leukemia Revealed by Single-Cell RNA Sequencing: Perspectives on Subtypes and Potential Therapeutic Targets.International journal of molecular sciences · 2025Article
- High oxidative phosphorylation represented by UQCRFS1 marks CD8 + tumor-infiltrating lymphocytes exhaustion in diffuse large B-cell lymphoma.Biology direct · 2025Article
- HDAC3-YY1-RAB5A axis remodels AML-supportive niche by modulating mitochondrial homeostasis in bone marrow stromal cells.Cell death & disease · 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
- The role and therapeutic potential of glucose metabolism in multidrug resistance of cancer.Frontiers in cell and developmental biology · 2025Review
- Review
- The role of glycolysis in tumorigenesis: From biological aspects to therapeutic opportunities.Neoplasia (New York, N.Y.) · 2024Review
- Altered metabolism in cancer: insights into energy pathways and therapeutic targets.Molecular cancer · 2024Review
- Gene regulatory network topology governs resistance and treatment escape in glioma stem-like cells.Science advances · 2024Article
- Functional characterization of cooperating MGA mutations in RUNX1::RUNX1T1 acute myeloid leukemia.Leukemia · 2024Article
- Low expression of miR-182 caused by DNA hypermethylation accelerates acute lymphocyte leukemia development by targeting PBX3 and BCL2: miR-182 promoter methylation is a predictive marker for hypomethylation agents + BCL2 inhibitor venetoclax.Clinical epigenetics · 2024Article
- RNA-seq-based miRNA signature as an independent predictor of relapse in pediatric B-cell acute lymphoblastic leukemia.Blood advances · 2024Article
- Endothelial-derived small extracellular vesicles support B-cell acute lymphoblastic leukemia development.Cellular oncology (Dordrecht, Netherlands) · 2024Article
- Microfluidics-free single-cell genomics with templated emulsification.Nature biotechnology · 2023Article
Corrections and comments
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Authors and funding
17 authors at 6 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
How metabolic status controls the fates of different types of leukemia cells remains elusive. Using a SoNar-transgenic mouse line, we demonstrated that B cell acute lymphoblastic leukemia (B-ALL) cells had a preference in using oxidative phosphorylation. B-ALL cells with a low SoNar ratio (SoNar-low) had enhanced mitochondrial respiration capacity, mainly resided in the vascular niche, and were enriched with more functional leukemia-initiating cells than that of SoNar-high cells in a murine B-ALL model. The SoNar-low cells were more resistant to cytosine arabinoside (Ara-C) treatment. cyclic adenosine 3',5'-monophosphate response element-binding protein transactivated pyruvate dehydrogenase complex component X and cytidine deaminase to maintain the oxidative phosphorylation level and Ara-C-induced resistance. SoNar-low human primary B-ALL cells also had a preference for oxidative phosphorylation. Suppressing oxidative phosphorylation with several drugs sufficiently attenuated Ara-C-induced resistance. Our study provides a unique angle for understanding the potential connections between metabolism and B-ALL cell fates.
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