ArticleLeukemia2022
GFI1B acts as a metabolic regulator in hematopoiesis and acute myeloid leukemia.
Article in Leukemia, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 24 citations in OpenAlex.
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- Impact of Acute Myeloid Leukemia Cells on the Metabolic Function of Bone Marrow Mesenchymal Stem Cells.International journal of molecular sciences · 2025Article
- High mtDNA content identifies oxidative phosphorylation-driven acute myeloid leukemias and represents a therapeutic vulnerability.Signal transduction and targeted therapy · 2025Article
- Emerging roles for fatty acid oxidation in cancer.Genes & diseases · 2025Review
- Germline Single-Nucleotide PolymorphismBiomedicines · 2025Article
- Reprogramming hematopoietic stem cell metabolism in lung cancer: glycolysis, oxidative phosphorylation, and the role of 2-DG.Biology direct · 2024Article
- Enhanced MCM5 Level Predicts Bad Prognosis in Acute Myeloid Leukemia.Molecular biotechnology · 2023Article
- Impaired Repopulating Ability ofGenes · 2023Article
- Spatio-temporal transcriptome dynamics coordinate rapid transition of core crop functions in 'lactating' pigeon.PLoS genetics · 2023Article
- [Establishment of leukemia cell model with inducible AML1-ETO expression and its effect on fatty acid metabolism in leukemia cells].Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi · 2023Article
- LSD1 inhibition modulates transcription factor networks in myeloid malignancies.Frontiers in oncology · 2023Review
- The microbiota metabolite, phloroglucinol, confers long-term protection against inflammation.Gut microbesArticle
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Authors and funding
19 authors at 6 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recent studies highlighted the role of transcription factors in metabolic regulation during hematopoiesis and leukemia development. GFI1B is a transcriptional repressor that plays a critical role in hematopoiesis, and its expression is negatively related to the prognosis of acute myeloid leukemia (AML) patients. We earlier reported a change in the metabolic state of hematopoietic stem cells upon Gfi1b deletion. Here we explored the role of Gfi1b in metabolism reprogramming during hematopoiesis and leukemogenesis. We demonstrated that Gfi1b deletion remarkably activated mitochondrial respiration and altered energy metabolism dependence toward oxidative phosphorylation (OXPHOS). Mitochondrial substrate dependency was shifted from glucose to fatty acids upon Gfi1b deletion via upregulating fatty acid oxidation (FAO). On a molecular level, Gfi1b epigenetically regulated multiple FAO-related genes. Moreover, we observed that metabolic phenotypes evolved as cells progressed from preleukemia to leukemia, and the correlation between Gfi1b expression level and metabolic phenotype was affected by genetic variations in AML cells. FAO or OXPHOS inhibition significantly impeded leukemia progression of Gfi1b-KO MLL/AF9 cells. Finally, we showed that Gfi1b-deficient AML cells were more sensitive to metformin as well as drugs implicated in OXPHOS and FAO inhibition, opening new potential therapeutic strategies.
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