ArticleOncogene2019
BET bromodomain inhibition blocks the function of a critical AR-independent master regulator network in lethal prostate cancer.
Article in Oncogene, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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.
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Who cites it
18 citing papers in PubMed, 27 citations in OpenAlex.
- A Phase Ib/IIa Study of the Pan-BET Inhibitor ZEN-3694 in Combination with Enzalutamide in Patients with Metastatic Castration-resistant Prostate Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2020Trial
- Combined BET bromodomain and DNA methyltransferase inhibition targets critical survival pathways in transdifferentiated prostate cancer.JCI insight · 2026Article
- E2F1 K117 methylation by SETD6 disrupts BRD4-E2F1 binding and modulates E2F1 chromatin binding and gene regulation in prostate cancer cells.Nucleic acids research · 2026Article
- Immunological facets of prostate cancer and the potential of immune checkpoint inhibition in disease management.Theranostics · 2024Review
- Simultaneous administration of EZH2 and BET inhibitors inhibits proliferation and clonogenic ability of metastatic prostate cancer cells.Journal of enzyme inhibition and medicinal chemistry · 2023Article
- Targeting CBX3 with a Dual BET/PLK1 Inhibitor Enhances the Antitumor Efficacy of CDK4/6 Inhibitors in Prostate Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Epigenetic (De)regulation in Prostate Cancer.Cancer treatment and research · 2023Article
- IL-1β expression driven by androgen receptor absence or inactivation promotes prostate cancer bone metastasis.Cancer research communications · 2022Article
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- BET Bromodomain Inhibition Blocks an AR-Repressed, E2F1-Activated Treatment-Emergent Neuroendocrine Prostate Cancer Lineage Plasticity Program.Clinical cancer research : an official journal of the American Association for Cancer Research · 2021Article
- The heterogeneity of prostate cancers lacking AR activity will require diverse treatment approaches.Endocrine-related cancer · 2021Review
- Recent Advances in Epigenetic Biomarkers and Epigenetic Targeting in Prostate Cancer.European urology · 2021Review
- MYC-Mediated Ribosomal Gene Expression Sensitizes Enzalutamide-resistant Prostate Cancer Cells to EP300/CREBBP Inhibitors.The American journal of pathology · 2021Article
- Alternative splicing of LSD1+8a in neuroendocrine prostate cancer is mediated by SRRM4.Neoplasia (New York, N.Y.) · 2020Article
- A census of pathway maps in cancer systems biology.Nature reviews. Cancer · 2020Review
- The combined effect of epigenetic inhibitors for LSD1 and BRD4 alters prostate cancer growth and invasion.Aging · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors at 1 institution in 1 country.
Funding
Abstract
BET bromodomain inhibitors block prostate cancer cell growth at least in part through c-Myc and androgen receptor (AR) suppression. However, little is known about other transcriptional regulators whose suppression contributes to BET bromodomain inhibitor anti-tumor activity. Moreover, the anti-tumor activity of BET bromodomain inhibition in AR-independent castration-resistant prostate cancers (CRPC), whose frequency is increasing, is also unknown. Herein, we demonstrate that BET bromodomain inhibition blocks growth of a diverse set of CRPC cell models, including those that are AR-independent or in which c-Myc is not suppressed. To identify transcriptional regulators whose suppression accounts for these effects, we treated multiple CRPC cell lines with the BET bromodomain inhibitor JQ1 and then performed RNA-sequencing followed by Master Regulator computational analysis. This approach identified several previously unappreciated transcriptional regulators that are highly expressed in CRPC and whose suppression, via both transcriptional or post-translational mechanisms, contributes to the anti-tumor activity of BET bromodomain inhibitors.
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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.