ArticleLeukemia2022
TET3 promotes AML growth and epigenetically regulates glucose metabolism and leukemic stem cell associated pathways.
Article in Leukemia, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.
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Who cites it
33 citing papers in PubMed, 1 synthesis or guideline pooled it, 37 citations in OpenAlex.
- Targeting Mitochondrial Oxidative Phosphorylation Eradicates Acute Myeloid Leukemic Stem Cells.Frontiers in oncology · 2022Pooled it
- Advances in natural killer cell immunotherapy for hematologic malignancies.Cancer biology & therapy · 2026Review
- Tumor cell-intrinsic TET3 restrains type I interferon signaling and anti-tumor immunity.Science China. Life sciences · 2026Article
- The metabolic profiles of cancer stem cells.Stem cell research & therapy · 2026Review
- Identification of glycolysis -correlative features for predicting prognosis and investigating immune landscape in prostate cancer.BMC cancer · 2026Article
- Epigenetics and One-Carbon Metabolism in Cancer: Mechanisms and Therapeutic Implications.Advances in experimental medicine and biology · 2026Review
- Activation of WDHD1 by DNA demethylases promotes MINPP1 transcription and glycolysis in lung adenocarcinoma progression.Respiratory research · 2025Article
- JMJD1C forms condensate to facilitate a RUNX1-dependent gene expression program shared by multiple types of AML cells.Protein & cell · 2025Article
- TET3 regulates hematopoietic stem cell homeostasis during embryonic and adult hematopoiesis.HemaSphere · 2025Article
- The role of glycolysis in tumorigenesis: From biological aspects to therapeutic opportunities.Neoplasia (New York, N.Y.) · 2024Review
- Unraveling the role of long non-coding RNAs in therapeutic resistance in acute myeloid leukemia: New prospects & challenges.Non-coding RNA research · 2024Review
- Metabolic dependencies of acute myeloid leukemia stem cells.International journal of hematology · 2024Review
- Article
- ncRNAs-mediated overexpression ofHeliyon · 2024Article
- TET2 mutation as prototypic clonal hematopoiesis lesion.Seminars in hematology · 2024Review
- Epigenetic regulation in cancer.MedComm · 2024Review
- Interplay between epigenetics and metabolism controls cancer stem cell plasticity.Frontiers in epigenetics and epigenomics · 2024Review
- The Quiet Giant: Identification, Effectors, Molecular Mechanism, Physiological and Pathological Function in mRNA 5-methylcytosine Modification.International journal of biological sciences · 2024Review
- Bidirectional interplay between metabolism and epigenetics in hematopoietic stem cells and leukemia.The EMBO journal · 2023Review
- Direct inhibition of dioxygenases TET1 by the rheumatoid arthritis drug auranofin selectively induces cancer cell death in T-ALL.Journal of hematology & oncology · 2023Article
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute myeloid leukemia (AML) is considered a poor prognosis malignancy where patients exhibit altered glucose metabolism and stem cell signatures that contribute to AML growth and maintenance. Here, we report that the epigenetic factor, Ten-Eleven Translocation 3 (TET3) dioxygenase is overexpressed in AML patients and functionally validated human leukemic stem cells (LSCs), is required for leukemic growth by virtue of its regulation of glucose metabolism in AML cells. In human AML cells, TET3 maintains 5-hydroxymethylcytosine (5hmC) epigenetic marks and expression of early myeloid progenitor program, critical glucose metabolism and STAT5A signaling pathway genes, which also positively correlate with TET3 expression in AML patients. Consequently, TET3 depletion impedes hexokinase activity and L-Lactate production in AML cells. Conversely, overexpression of TET3 in healthy human hematopoietic stem progenitors (HSPCs) upregulates the expression of glucose metabolism, STAT5A signaling and AML associated genes, and impairs normal HSPC lineage differentiation in vitro. Finally, TET3 depletion renders AML cells highly sensitive to blockage of the TET3 downstream pathways glycolysis and STAT5 signaling via the combination of 2-Deoxy-D-glucose and STAT5 inhibitor which preferentially targets AML cells but spares healthy CD34
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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.