ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025
A Super-Enhancer-Driven Transcriptional Regulatory Circuit Underlying Abiraterone Resistance in Castration-Resistant Prostate Cancer.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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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
5 citing papers in PubMed.
- Article
- A Non-Canonical Core Transcriptional Regulatory Circuit Orchestrates Chromatin Reprogramming to Drive Osimertinib Resistance in Non-Small Cell Lung Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Super-enhancer-driven TCF4 orchestrates neuroblastoma metastasis by sphingolipid-dependent membrane remodeling and ITGB1-FAK activation.Neuro-oncology · 2026Article
- Targeting tumor transition windows.Exploration of targeted anti-tumor therapy · 2026Review
- A Super-Enhancer-Driven Transcriptional Regulatory Circuit Underlying Abiraterone Resistance in Castration-Resistant Prostate Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
Corrections and comments
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Authors and funding
19 authors.
Funding
Abstract
Castration-resistant prostate cancer (CRPC) remains the leading cause of mortality among prostate cancer patients. While second-generation androgen receptor (AR) pathway-targeted therapies, such as Abiraterone, have significantly improved survival outcomes, resistance to these treatments ultimately emerges, posing a critical challenge. Understanding the mechanisms underlying Abiraterone resistance is essential for developing strategies to enhance patient outcomes. In this study, a super-enhancer (SE)-driven transcriptional regulatory circuit is identified involving BCL6, NFIB, and SMAD3 that facilitates Abiraterone resistance in CRPC. Through comprehensive analyses of SE expression profiles in Abiraterone-resistant CRPC cells and their parental counterparts, it is revealed that this circuit plays a pivotal role in resistance progression. Mechanistically, BCL6, NFIB, and SMAD3 synergistically remodel the transcriptional landscape of resistant CRPC cells, driving resistance by regulating cholesterol biosynthesis and cell cycle pathways. The findings provide critical insights into the transcriptional dysregulation underlying Abiraterone resistance and highlight potential therapeutic strategies to counteract treatment resistance in CRPC, ultimately aiming to improve patient survival and quality of life.
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Registered trials
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