ArticleOncogene2014
MYC, a downstream target of BRD-NUT, is necessary and sufficient for the blockade of differentiation in NUT midline carcinoma.
Article in Oncogene, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 117 papers.
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Who cites it
117 citing papers in PubMed, 184 citations in OpenAlex.
- BRD proteins in human retroviral infection: emerging evidence from HIV-1 and future perspectives for HTLV-1.Molecular biology reports · 2026Review
- Eyes Toward the Clinic: Selective Inhibition and Degradation Approaches to Bromodomain-Containing Proteins.Chembiochem : a European journal of chemical biology · 2026Review
- NSD3 stabilizes nuclear compartmentalization and promotes megabase-scale chromatin interactions.bioRxiv : the preprint server for biology · 2026Article
- International guidelines on the diagnosis and treatment of NUT carcinoma.Innovation (Cambridge (Mass.)) · 2026Review
- Magnifying Glass on Sinonasal NUT Carcinoma Heterogeneity via Spatial Transcriptomics.Head & neck · 2026Article
- Targeting oncogenic fusion-driven NUT carcinoma with CRISPR-Cas9 genome editing.Molecular therapy. Oncology · 2025Article
- Tumor microenvironment-targeted PROTAC nanoparticle self-assembly broadly predicted by structural descriptors.Science advances · 2025Article
- NSD3::NUTM1 fusion evidenced on RNA sequencing in poorly differentiated thyroid cancer: a report of two cases.European thyroid journal · 2025Article
- Molecular Characterization of NUT Carcinoma: A Report from the NUT Carcinoma Registry.Clinical cancer research : an official journal of the American Association for Cancer Research · 2025Article
- Hiding in plain sight: NUT carcinoma is an unrecognized subtype of squamous cell carcinoma of the lungs and head and neck.Nature reviews. Clinical oncology · 2025Review
- Review
- Chem-CRISPR/dCas9FCPF: a platform for chemically induced epigenome editing.Nucleic acids research · 2024Article
- A Review of the Bromodomain and Extraterminal Domain Epigenetic Reader Proteins: Function on Virus Infection and Cancer.Viruses · 2024Review
- Article
- [NUT cancer of nasal cavity and sinuses: a case report and literature review].Lin chuang er bi yan hou tou jing wai ke za zhi = Journal of clinical otorhinolaryngology head and neck surgery · 2024Review
- Multimodal Therapy Approaches for NUT Carcinoma by Dual Combination of Oncolytic VirusViruses · 2024Article
- Initial Chemotherapy for Locally Advanced and Metastatic NUT Carcinoma.Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer · 2024Article
- Top IHC/ISH Hacks for and Molecular Surrogates of Poorly Differentiated Sinonasal Small Round Cell Tumors.Head and neck pathology · 2024Review
- Combined BET and MEK Inhibition synergistically suppresses melanoma by targeting YAP1.Theranostics · 2024Article
- Metabolic and Epigenetic Reprogramming in a Case of Nuclear Protein in Testis (NUT) Carcinoma of the Retroperitoneum.Cureus · 2024Article
57 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 4 institutions in 2 countries.
Funding
Abstract
NUT midline carcinoma (NMC) is an aggressive type of squamous cell carcinoma that is defined by the presence of BRD-NUT fusion oncogenes, which encode chimeric proteins that block differentiation and maintain tumor growth. BRD-NUT oncoproteins contain two bromodomains whose binding to acetylated histones is required for the blockade of differentiation in NMC, but the mechanisms by which BRD-NUT act remain uncertain. Here, we provide evidence that MYC is a key downstream target of BRD4-NUT. Expression profiling of NMCs shows that the set of genes whose expression is maintained by BRD4-NUT is highly enriched for MYC upregulated genes, and MYC and BRD4-NUT protein expression is strongly correlated in primary NMCs. More directly, we find that BRD4-NUT associates with the MYC promoter and is required to maintain MYC expression in NMC cell lines. Moreover, both siRNA knockdown of MYC and a dominant-negative form of MYC, omomyc, induce differentiation of NMC cells. Conversely, differentiation of NMC cells induced by knockdown of BRD4-NUT is abrogated by enforced expression of MYC. Together, these findings suggest that MYC is a downstream target of BRD4-NUT that is required for maintenance of NMC cells in an undifferentiated, proliferative state. Our findings support a model in which dysregulation of MYC by BRD-NUT fusion proteins has a central role in the pathogenesis of NMC.
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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.