ArticleBreast cancer research and treatment2015
Inhibition of BET proteins impairs estrogen-mediated growth and transcription in breast cancers by pausing RNA polymerase advancement.
Article in Breast cancer research and treatment, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 36 citations in OpenAlex.
- Combinational BET and mTOR inhibition unveils EGR1 as acute myeloid leukemia prognostic biomarker.Scientific reports · 2025Article
- Resistance of estrogen receptor function to BET bromodomain inhibition is mediated by transcriptional coactivator cooperativity.Nature structural & molecular biology · 2025Article
- BET Bromodomain Inhibition Potentiates Ocular Melanoma Therapy by Inducing Cell Cycle Arrest.Investigative ophthalmology & visual science · 2024Article
- Genome-Wide Estrogen Receptor Activity in Breast Cancer.Endocrinology · 2021Review
- The emerging role of BET inhibitors in breast cancer.Breast (Edinburgh, Scotland) · 2020Review
- Novel Pyrrolopyridone Bromodomain and Extra-Terminal Motif (BET) Inhibitors Effective in Endocrine-Resistant ER+ Breast Cancer with Acquired Resistance to Fulvestrant and Palbociclib.Journal of medicinal chemistry · 2020Article
- Review
- Compound C620-0696, a new potent inhibitor targeting BPTF, the chromatin-remodeling factor in non-small-cell lung cancer.Frontiers of medicine · 2020Article
- Combining epigenetic drugs with other therapies for solid tumours - past lessons and future promise.Nature reviews. Clinical oncology · 2020Review
- Distinct Roles for BET Family Members in Estrogen Receptor α Enhancer Function and Gene Regulation in Breast Cancer Cells.Molecular cancer research : MCR · 2019Article
- Estrogen-Induced Apoptosis in Breast Cancers Is Phenocopied by Blocking Dephosphorylation of Eukaryotic Initiation Factor 2 Alpha (eIF2α) Protein.Molecular cancer research : MCR · 2019Article
- Inhibition of BET Proteins and Histone Deacetylase (HDACs): Crossing Roads in Cancer Therapy.Cancers · 2019Review
- Targeting BRD4 proteins suppresses the growth of NSCLC through downregulation of eIF4E expression.Cancer biology & therapy · 2018Article
- Targeting bromodomain and extraterminal proteins in breast cancer.Pharmacological research · 2018Review
- BET inhibitors as novel therapeutic agents in breast cancer.Oncotarget · 2017Review
- Transcriptional Dependencies in Diffuse Intrinsic Pontine Glioma.Cancer cell · 2017Article
- Review
- Targeted Degradation of BET Proteins in Triple-Negative Breast Cancer.Cancer research · 2017Article
- A Novel Epi-drug Therapy Based on the Suppression of BET Family Epigenetic Readers.The Yale journal of biology and medicine · 2017Review
- AR Signaling in Breast Cancer.Cancers · 2017Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
Estrogen (E2)-induced transcription requires coordinated recruitment of estrogen receptor α (ER) and multiple factors at the promoter of activated genes. However, the precise mechanism by which this complex stimulates the RNA polymerase II activity required to execute transcription is largely unresolved. We investigated the role of bromodomain (BRD) containing bromodomain and extra-terminal (BET) proteins, in E2-induced growth and gene activation. JQ1, a specific BET protein inhibitor, was used to block BET protein function in two different ER-positive breast cancer cell lines (MCF7 and T47D). Real-time PCR and ChIP assays were used to measure RNA expression and to detect recruitment of various factors on the genes, respectively. Protein levels were measured by Western blotting. JQ1 suppressed E2-induced growth and transcription in both MCF7 and T47D cells. The combination of E2 and JQ1 down-regulated the levels of ER protein in MCF7 cells but the loss of ER was not responsible for JQ1-mediated inhibition of E2 signaling. JQ1 did not disrupt E2-induced recruitment of ER and co-activator (SRC3) at the E2-responsive DNA elements. The E2-induced increase in histone acetylation was also not altered by JQ1. However, JQ1 blocked the E2-induced transition of RNA polymerase II from initiation to elongation by stalling it at the promoter region of the responsive genes upstream of the transcription start site. This study establishes BET proteins as the key mediators of E2-induced transcriptional activation. This adds another layer of complexity to the regulation of estrogen-induced gene activation that can potentially be targeted for therapeutic intervention.
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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.