ArticleProceedings of the National Academy of Sciences of the United States of America2017
Uncovering BRD4 hyperphosphorylation associated with cellular transformation in NUT midline carcinoma.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 63 citations in OpenAlex.
- BRD4: From molecular understanding to therapeutics development.Molecular cell · 2026Review
- The oncolytic vesicular stomatitis virus VSV-GP shows profound oncolytic activity in NUT-carcinoma cell lines.Molecular therapy. Oncology · 2026Article
- Recruitment of BRD4 to the ASXL1 genomic targets depends on the extra-terminal domain of BRD4.Nature communications · 2026Article
- Gαq-Stimulated Gene Expression Is Insensitive to Bromo Extra Terminal Domain Inhibitors in HEK 293 Cells.International journal of molecular sciences · 2025Article
- Cyclin-dependent kinases as mediators of aberrant transcription in prostate cancer.Translational oncology · 2025Review
- A Minireview on BET Inhibitors: Beyond Bromodomain Targeting.Biomedicines · 2025Review
- CDK9 inhibition inhibits multiple oncogenic transcriptional and epigenetic pathways in prostate cancer.British journal of cancer · 2024Article
- An updated patent review of BRD4 degraders.Expert opinion on therapeutic patents · 2024Review
- Elevating PLK1 overcomes BETi resistance in prostate cancer via triggering BRD4 phosphorylation-dependent degradation in mitosis.Cell reports · 2024Article
- Targeting BRD4: Potential therapeutic strategy for head and neck squamous cell carcinoma (Review).Oncology reports · 2024Article
- Application of Nanoparticles in the Diagnosis and Treatment of Colorectal Cancer.Anti-cancer agents in medicinal chemistry · 2024Review
- Bromodomain and extraterminal (BET) proteins: biological functions, diseases, and targeted therapy.Signal transduction and targeted therapy · 2023Review
- BRD4 and MYC: power couple in transcription and disease.The FEBS journal · 2023Review
- Prolonged Survival of NUT Midline Carcinoma and Current Approaches to Treatment.The oncologist · 2023Article
- Integration of Chemoinformatics and Multi-Omics Analysis Defines ECT2 as a Potential Target for Cancer Drug Therapy.Biology · 2023Article
- Accurate Prediction of Transcriptional Activity of Single Missense Variants in HIV Tat with Deep Learning.International journal of molecular sciences · 2023Article
- Structural mechanism of BRD4-NUT and p300 bipartite interaction in propagating aberrant gene transcription in chromatin in NUT carcinoma.Nature communications · 2023Article
- EGFR-induced suppression of HPV E6/E7 is mediated by microRNA-9-5p silencing of BRD4 protein in HPV-positive head and neck squamous cell carcinoma.Cell death & disease · 2022Article
- Targeting cyclin-dependent kinase 9 in cancer therapy.Acta pharmacologica Sinica · 2022Review
- NUT midline carcinoma as a primary lung tumor treated with anlotinib combined with palliative radiotherapy: a case report.Diagnostic pathology · 2022Article
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
The epigenetic reader BRD4 plays a vital role in transcriptional regulation, cellular growth control, and cell-cycle progression. Dysregulation of BRD4 function has been implicated in the pathogenesis of a wide range of cancers. However, how BRD4 is regulated to maintain its normal function in healthy cells and how alteration of this process leads to cancer remain poorly understood. In this study, we discovered that BRD4 is hyperphosphorylated in NUT midline carcinoma and identified CDK9 as a potential kinase mediating BRD4 hyperphosphorylation. Disruption of BRD4 hyperphosphorylation using both chemical and molecular inhibitors led to the repression of BRD4 downstream oncogenes and abrogation of cellular transformation. BRD4 hyperphosphorylation is also observed in other cancers displaying enhanced BRD4 oncogenic activity. Our study revealed a mechanism that may regulate BRD4 biological function through phosphorylation, which, when dysregulated, could lead to oncogenesis. Our finding points to strategies to target the aberrant BRD4 signaling specifically for cancer intervention.
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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.