ReviewCell death discovery2023
Super-enhancers and the super-enhancer reader BRD4: tumorigenic factors and therapeutic targets.
Review in Cell death discovery, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
65 citing papers in PubMed, 78 citations in OpenAlex.
- The DCBLD2 super-enhancer drives colorectal cancer progression through FOSL2/JUND-mediated activation of the CD146/AKT/TNFRSF6B pathway.Molecular biomedicine · 2026Article
- Histone modifications: mechanisms, metabolic regulation, and therapeutic targeting in cancer.Precision clinical medicine · 2026Review
- Glucose and Glutamine Deprivation Promotes Breast Cancer Lung Metastasis via BRD4-Dependent Enhancer Activation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Engineered bacteria as exogenous organelle mimics restore PTEN and p53 tumor suppressor functions for cancer therapy.Nature communications · 2026Article
- Transcription factor targeting strategies in cancer: mechanisms, challenges and cutting-edge progress.Acta pharmacologica Sinica · 2026Review
- Advances in Mechanism of Action and Efficacy of CBP/p300 Inhibitors in Different Subtypes of Breast Cancer.Molecules (Basel, Switzerland) · 2026Review
- Article
- Acetylation in ovarian cancer: mechanistic insights into drug resistance and emerging therapeutic opportunities.Journal of ovarian research · 2026Review
- Cis and trans regulatory mechanisms of extrachromosomal DNA segregation.Nature cell biology · 2026Article
- Hierarchical interplay between H3K27ac and H3K4me3 in transcriptional regulation.Nature communications · 2026Article
- Epigenetic regulation in atherosclerosis and its therapeutic potential.Nature reviews. Cardiology · 2026Review
- Mapping of the hSOX10 Proximal Protein Interactome in Human Melanoma.Journal of proteome research · 2026Article
- Perturbation of BRD4 and p300 activity suppresses super enhancer‑drivenOncology reports · 2026Article
- 3D chromatin architecture in cancer: mechanisms of dysregulation and emerging therapeutic strategies.Experimental & molecular medicine · 2026Review
- Super-enhancer-driven KIAA1522 upregulation suppresses ferroptosis in hepatocellular carcinoma.Clinical and translational medicine · 2026Article
- Super-enhancer-driven LncRNA MIR205HG promotes esophageal squamous cell carcinoma progression via glycolysis reprogramming.Journal of translational medicine · 2026Article
- Epigenetic modifications in cancer drug resistance: molecular mechanisms and therapeutic interventions.Molecular biomedicine · 2026Review
- Targeting a super-enhancer induced aldehyde dehydrogenase metabolic loop mitigates CDK4/6 inhibitor resistance in estrogen receptor-positive cancers.Nature communications · 2026Article
- Review
- Targeting BRD4-A Promising Therapeutic Option for Glioblastoma?International journal of molecular sciences · 2026Review
5 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
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Transcriptional super-enhancers and the BET bromodomain protein BRD4 are emerging as critical drivers of tumorigenesis and therapeutic targets. Characterized by substantial accumulation of histone H3 lysine 27 acetylation (H3K27ac) signals at the loci of cell identity genes and critical oncogenes, super-enhancers are recognized, bound and activated by BRD4, resulting in considerable oncogene over-expression, malignant transformation, cancer cell proliferation, survival, tumor initiation and progression. Small molecule compound BRD4 BD1 and BD2 bromodomain inhibitors block BRD4 binding to super-enhancers, suppress oncogene transcription and expression, reduce cancer cell proliferation and survival, and repress tumor progression in a variety of cancer types. Like other targeted therapy agents, BRD4 inhibitors show moderate anticancer effects on their own, and exert synergistic anticancer effects in vitro and in preclinical models, when combined with other anticancer agents including CDK7 inhibitors, CBP/p300 inhibitors and histone deacetylase inhibitors. More recently, BRD4 BD2 bromodomain selective inhibitors, proteolysis-targeting chimera (PROTAC) BRD4 protein degraders, and dual BRD4 and CBP/p300 bromodomain co-inhibitors have been developed and shown better anticancer efficacy and/or safety profile. Importantly, more than a dozen BRD4 inhibitors have entered clinical trials in patients with cancer of various organ origins. In summary, super-enhancers and their reader BRD4 are critical tumorigenic drivers, and BRD4 BD1 and BD2 bromodomain inhibitors, BRD4 BD2 bromodomain selective inhibitors, PROTAC BRD4 protein degraders, and dual BRD4 and CBP/p300 bromodomain co-inhibitors are promising novel anticancer agents for clinical translation.
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.