ArticleOncogenesis2012
Genome-wide profiling reveals transcriptional repression of MYC as a core component of NR4A tumor suppression in acute myeloid leukemia.
Article in Oncogenesis, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
23 citing papers in PubMed, 55 citations in OpenAlex.
- PROTAC-mediated targeting of IKKβ and NR4A1 for AML therapy.Oncogene · 2026Article
- Targeting Lineage-Specific Functions of NR4A1 for Cancer Immunotherapy.International journal of molecular sciences · 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
- Z-ligustilide preferentially caused mitochondrial dysfunction in AML HL-60 cells by activating nuclear receptors NUR77 and NOR1.Chinese medicine · 2023Article
- Druggability Evaluation of the Neuron Derived Orphan Receptor (NOR-1) Reveals Inverse NOR-1 Agonists.ChemMedChem · 2022Article
- Role of NR4A family members in myeloid cells and leukemia.Current research in immunology · 2022Article
- Comprehensive insights into the function and molecular and pharmacological regulation of neuron-derived orphan receptor 1, an orphan receptor.Frontiers in pharmacology · 2022Review
- The non-coding genome in genetic brain disorders: new targets for therapy?Essays in biochemistry · 2021Review
- Targeting NR4A Nuclear Receptors to Control Stromal Cell Inflammation, Metabolism, Angiogenesis, and Tumorigenesis.Frontiers in cell and developmental biology · 2021Review
- Targeting Oncogenic Super Enhancers in MYC-Dependent AML Using a Small Molecule Activator of NR4A Nuclear Receptors.Scientific reports · 2020Article
- Cantharidin Induces Apoptosis and Promotes Differentiation of AML Cells Through Nuclear Receptor Nur77-Mediated Signaling Pathway.Frontiers in pharmacology · 2020Article
- Function of Nr4a Orphan Nuclear Receptors in Proliferation, Apoptosis and Fuel Utilization Across Tissues.Cells · 2019Review
- Fenretinide-induced Apoptosis of Acute Myeloid Leukemia Cells via NR4A1 Translocation into Mitochondria and Bcl-2 Transformation.Journal of Cancer · 2019Article
- Article
- NR4A1 and NR4A3 restrict HSC proliferation via reciprocal regulation of C/EBPα and inflammatory signaling.Blood · 2018Article
- Nur77 Is Upregulated in B-1a Cells by Chronic Self-Antigen Stimulation and Limits Generation of Natural IgM Plasma Cells.ImmunoHorizons · 2017Article
- Dual Inhibition of EZH2 and EZH1 Sensitizes PRC2-Dependent Tumors to Proteasome Inhibition.Clinical cancer research : an official journal of the American Association for Cancer Research · 2017Article
- BINDING SITE ANALYSIS OF THENuclear receptor research · 2017Article
- Possible role of intragenic DNA hypermethylation in gene silencing of the tumor suppressor gene NR4A3 in acute myeloid leukemia.Leukemia research · 2016Article
- Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Acute myeloid leukemias (AMLs) are a heterogeneous group of diseases that are sustained by relatively rare leukemia-initiating cells (LICs) that exhibit diverse genetic and phenotypic properties. AML heterogeneity presents a major challenge to development of targeted therapies, and effective treatment will require targeting of common molecular drivers of AML maintenance. The orphan nuclear receptors NR4A1 and NR4A3 are potent tumor suppressors of AML. They are silenced in all human AML LICs, irrespective of patient cytogenetics, and their deletion in mice leads to postnatal AML development. In the current report, we address the tumor-suppressive mechanisms and therapeutic potential of NR4As for AML intervention. We show that rescue of either NR4A1 or NR4A3 inhibits the leukemogenicity of AML cells in vivo and reprograms a subset of gene signatures that distinguish primary human LICs from normal hematopoietic stem cells (HSCs), irrespective of subtype. Central to NR4A reprogramming is the acute suppression of an LIC submodule that includes the transcriptional repression of MYC. Additionally, we show that upregulation of MYC is an acute preleukemic consequence of NR4A deletion and that MYC suppression functionally contributes to NR4A antileukemic effects. Collectively, these results identify NR4As as novel targets for AML therapeutic intervention and reveal molecular targets of NR4A tumor suppression, including the suppression of MYC.
Identifiers
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.