ArticleClinical cancer research : an official journal of the American Association for Cancer Research2019
Functional and Mechanistic Interrogation of BET Bromodomain Degraders for the Treatment of Metastatic Castration-resistant Prostate Cancer.
Article in Clinical cancer research : an official journal of the American Association for Cancer Research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 33 citations in OpenAlex.
- A non-enzymatic role for METTL3 as an Androgen Receptor co-regulator that promotes prostate cancer proliferation.bioRxiv : the preprint server for biology · 2026Article
- Cancer stem cell plasticity in shaping drug resistance landscapes in prostate cancer.Journal of advanced research · 2026Review
- Targeting histone H2B acetylated enhanceosomes via p300/CBP degradation in prostate cancer.Nature genetics · 2025Article
- Simultaneous inhibition of TRIM24 and TRIM28 sensitises prostate cancer cells to antiandrogen therapy, decreasing VEGF signalling and angiogenesis.Molecular oncology · 2025Article
- Article
- The Homeobox Transcription Factor NKX3.1 Displays an Oncogenic Role in Castration-Resistant Prostate Cancer Cells.Cancers · 2025Article
- The role of TXNIP in cancer: a fine balance between redox, metabolic, and immunological tumor control.British journal of cancer · 2023Review
- BCR-ABL triggers a glucose-dependent survival program during leukemogenesis through the suppression of TXNIP.Cell death & disease · 2023Article
- Epigenetic (De)regulation in Prostate Cancer.Cancer treatment and research · 2023Article
- Editorial: Hormone resistance in cancer.Frontiers in endocrinology · 2023Article
- Article
- The genetic heterogeneity and drug resistance mechanisms of relapsed refractory multiple myeloma.Nature communications · 2022Article
- The Integration of Metabolomics with Other Omics: Insights into Understanding Prostate Cancer.Metabolites · 2022Review
- Thioredoxin-Interacting Protein in Cancer and Diabetes.Antioxidants & redox signaling · 2022Review
- Dual inhibition of BET and HAT/p300 suppresses colorectal cancer via DR5- and p53/PUMA-mediated cell death.Frontiers in oncology · 2022Article
- Preclinical and Clinical Advances of Targeted Protein Degradation as a Novel Cancer Therapeutic Strategy: An Oncologist Perspective.Targeted oncology · 2021Review
- Applications of Lipidomics in Tumor Diagnosis and Therapy.Advances in experimental medicine and biology · 2021Article
- Cellular rewiring in lethal prostate cancer: the architect of drug resistance.Nature reviews. Urology · 2020Review
- Androgen receptor degraders overcome common resistance mechanisms developed during prostate cancer treatment.Neoplasia (New York, N.Y.) · 2020Article
- The combined effect of epigenetic inhibitors for LSD1 and BRD4 alters prostate cancer growth and invasion.Aging · 2020Article
Corrections and comments
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Authors and funding
15 authors at 1 institution in 1 country.
Funding
Abstract
purposeThe bromodomain and extraterminal (BET)-containing proteins (BRD2/3/4) are essential epigenetic coregulators for prostate cancer growth. BRD inhibitors have shown promise for treatment of metastatic castration-resistant prostate cancer (mCRPC), and have been shown to function even in the context of resistance to next-generation AR-targeted therapies such as enzalutamide and abiraterone. Their clinical translation, however, has been limited by off-target effects, toxicity, and rapid resistance. EXPERIMENTAL
designWe have developed a series of molecules that target BET bromodomain proteins through their proteasomal degradation, improving efficacy and specificity of standard inhibitors. We tested their efficacy by utilizing prostate cancer cell lines and patient-derived xenografts, as well as several techniques including RNA-sequencing, mass spectroscopic proteomics, and lipidomics.
resultsBET degraders function
conclusionsCompounds inducing the pharmacologic degradation of BET proteins effectively target the major oncogenic drivers of prostate cancer, and ultimately present a potential advance in the treatment of mCRPC. In particular, our compound dBET-3, is most suited for further clinical development.
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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.