ArticleScientific reports2020
Targeting Oncogenic Super Enhancers in MYC-Dependent AML Using a Small Molecule Activator of NR4A Nuclear Receptors.
Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
24 citing papers in PubMed, 1 synthesis or guideline pooled it, 29 citations in OpenAlex.
- NR4A Family Genes: A Review of Comprehensive Prognostic and Gene Expression Profile Analysis in Breast Cancer.Frontiers in oncology · 2022Pooled it
- CRISPR Interference to Inhibit Oncogenes for Cancer Therapy.International journal of molecular sciences · 2026Review
- Remics: a redescription-based framework for multi-omics analysis.Frontiers in cell and developmental biology · 2026Article
- Ischemic stroke altered the expression profiles of super enhancer RNAs in mouse brain in a sexually dimorphic manner.Experimental neurology · 2025Article
- A Relapsed AML Case Featuring MYC and MECOM Rearrangements.Diagnostics (Basel, Switzerland) · 2025Article
- Biological roles of enhancer RNA m6A modification and its implications in cancer.Cell communication and signaling : CCS · 2025Review
- Innovative evaluation of selinexor and JQ1 synergy in leukemia therapy via C-MYC inhibition.Journal of translational medicine · 2025Article
- Super enhancers as key drivers of gene regulatory networks in normal and malignant hematopoiesis.Frontiers in cell and developmental biology · 2025Review
- Single-molecule RNA-FISH analysis reveals stochasticity in reactivation of latent HIV-1 regulated by Nuclear Orphan Receptors NR4A and cMYC.Research square · 2024Article
- Drug repurposing and prediction of multiple interaction types via graph embedding.BMC bioinformatics · 2023Article
- Review
- Super enhancers: Pathogenic roles and potential therapeutic targets for acute myeloid leukemia (AML).Genes & diseases · 2022Review
- Krüppel-like Factor 4 Supports the Expansion of Leukemia Stem Cells in MLL-AF9-driven Acute Myeloid Leukemia.Stem cells (Dayton, Ohio) · 2022Article
- Druggability Evaluation of the Neuron Derived Orphan Receptor (NOR-1) Reveals Inverse NOR-1 Agonists.ChemMedChem · 2022Article
- Review
- NR4A1 promotes LEF1 expression in the pathogenesis of papillary thyroid cancer.Cell death discovery · 2022Article
- Review
- NR4A1-3 nuclear receptor activity and immune cell dysregulation in rheumatic diseases.Frontiers in medicine · 2022Review
- Role of NR4A family members in myeloid cells and leukemia.Current research in immunology · 2022Article
- Regulation of 3D Organization and Its Role in Cancer Biology.Frontiers in cell and developmental biology · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Epigenetic reprogramming in Acute Myeloid Leukemia (AML) leads to the aberrant activation of super enhancer (SE) landscapes that drive the expression of key oncogenes, including the oncogenic MYC pathway. These SEs have been identified as promising therapeutic targets, and have given rise to a new class of drugs, including BET protein inhibitors, which center on targeting SE activity. NR4A nuclear receptors are tumor suppressors of AML that function in part through transcriptional repression of the MYC-driven oncogenic program via mechanisms that remain unclear. Here we show that NR4A1, and the NR4A inducing drug dihydroergotamine (DHE), regulate overlapping gene expression programs in AML and repress transcription of a subset of SE-associated leukemic oncogenes, including MYC. NR4As interact with an AML-selective SE cluster that governs MYC transcription and decommissions its activation status by dismissing essential SE-bound coactivators including BRD4, Mediator and p300, leading to loss of p300-dependent H3K27 acetylation and Pol 2-dependent eRNA transcription. DHE shows similar efficacy to the BET inhibitor JQ1 at repressing SE-dependent MYC expression and AML growth in mouse xenografts. Thus, DHE induction of NR4As provides an alternative strategy to BET inhibitors to target MYC dependencies via suppression of the AML-selective SE governing MYC expression.
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What OpenQuestion holds
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.