ArticleExperimental hematology & oncology2024
A novel AML1-ETO/FTO positive feedback loop promotes leukemogenesis and Ara-C resistance via stabilizing IGFBP2 in t(8;21) acute myeloid leukemia.
Article in Experimental hematology & oncology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 20 citations in OpenAlex.
- The role, regulatory mechanisms, and therapeutic implications of FTO in gastrointestinal cancer.Genes & diseases · 2026Review
- From pumps to networks: ABC transporters in leukemia resistance and microenvironmental adaptation.Medical oncology (Northwood, London, England) · 2026Review
- Integrative multi-omics, machine learning, and experimental validation reveal that TPM1 suppresses M2 macrophage polarization and enhances chemosensitivity in acute myeloid leukemia.Cell biology and toxicology · 2026Article
- Clinical characteristics and prognosis of therapy-related acute myeloid leukemia patients with RUNX1::RUNX1T1.BMC cancer · 2026Article
- FOXO1 in cancer: context-dependent roles, microRNA regulation, and therapeutic opportunities.Discover oncology · 2026Review
- Fusion oncoproteins orchestrate tumorigenesis and sustain malignant progression via a positive feedback mechanism.Cell & bioscience · 2026Review
- Nomogram-based prediction models for clinical outcomes in pediatricFrontiers in oncology · 2026Article
- Identification of a m6A-immune-related risk model for predicting prognosis, immune microenvironment, and drug responses in acute myeloid leukemia.Scientific reports · 2025Article
- FTO depletion does not alter mbioRxiv : the preprint server for biology · 2025Article
- Altered Expression of m6A-Associated Genes Is Linked with Poor Prognosis in Pediatric Acute Myeloid Leukemia Patients.Biomolecules · 2025Article
- Glycolysis Induces Abnormal Transcription Through Histone Lactylation in T-cell Acute Lymphoblastic Leukemia.Genomics, proteomics & bioinformatics · 2025Article
- Research progress on N6-methyladenosine and non-coding RNA in multiple myeloma.Discover oncology · 2025Review
- MMP14 from BM-MSCs facilitates progression and Ara-C resistance in acute myeloid leukemia via the JAK/STAT pathway.Experimental hematology & oncology · 2025Article
- Article
- Off-Target Inhibition of Human Dihydroorotate Dehydrogenase (ACS pharmacology & translational science · 2024Article
- A new perspective on hematological malignancies: m6A modification in immune microenvironment.Frontiers in immunology · 2024Review
Corrections and comments
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Authors and funding
11 authors at 5 institutions in 2 countries.
Funding
Abstract
backgroundt(8;21)(q22;q22) is one of the most frequent chromosomal abnormalities in acute myeloid leukemia (AML), leading to the generation of the fusion protein AML1-ETO. Despite t(8;21) AML being considered as a subtype with a favorable prognosis, approximately 30-50% of patients experience drug resistance and subsequent relapse. N
methodsChromatin immunoprecipitation, dual-luciferase reporter assay, m
resultsHere we show that FTO is highly expressed in t(8;21) AML, especially in patients with primary refractory disease. The expression of FTO is positively correlated with AML1-ETO, which is attributed to a positive regulatory loop between the AML1-ETO and FTO. Mechanistically, AML1-ETO upregulates FTO expression through inhibiting the transcriptional repression of FTO mediated by PU.1. Meanwhile, FTO promotes the expression of AML1-ETO by inhibiting YTHDF2-mediated AML1-ETO mRNA decay. Inactivation of FTO significantly suppresses cell proliferation, promotes cell differentiation and renders resistant t(8;21) AML cells sensitive to Ara-C. FTO exerts functions by regulating its mRNA targets, especially IGFBP2, in an m
conclusionOur work reveals a therapeutic potential of targeting AML1-ETO/FTO/IGFBP2 minicircuitry in the treatment for t(8;21) patients with resistance to Ara-C.
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