ArticleCell death discovery2022
High-dose-androgen-induced autophagic cell death to suppress the Enzalutamide-resistant prostate cancer growth via altering the circRNA-BCL2/miRNA-198/AMBRA1 signaling.
Article in Cell death discovery, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 18 citations in OpenAlex.
- Hsa_circ_0030568 Promotes the Proliferation and Migration of Prostate Cancer CellsCombinatorial chemistry & high throughput screening · 2026Article
- Programmed Cell Death in Cancer.MedComm · 2025Review
- AMBRA1 Inhibits Non-Small Cell Lung Cancer Progression Through miR-1178/p53/CDK2-Regulated Cell Cycle Arrest.Journal of cellular and molecular medicine · 2025Article
- Multiple roles of circular RNAs in prostate cancer: from the biological basis to potential clinical applications.European journal of medical research · 2025Review
- Role of circular RNAs in cancer therapy resistance.Molecular cancer · 2025Review
- A novel peptide encoded by circSRCAP confers resistance to enzalutamide by inhibiting the ubiquitin-dependent degradation of AR-V7 in castration-resistant prostate cancer.Journal of translational medicine · 2025Article
- Castration-resistant prostate cancer is resensitized to androgen deprivation by autophagy-dependent apoptosis induced by blocking SKP2.Science signaling · 2024Article
- Therapeutic importance and diagnostic function of circRNAs in urological cancers: from metastasis to drug resistance.Cancer metastasis reviews · 2024Review
- Role of Circular RNAs in Prostate Cancer.Current medicinal chemistry · 2024Review
- Small Mitochondria-Targeting Fluorophore with Multifunctional Therapeutic Activities against Prostate Cancer via the HIF1α/OATPs Pathway.Molecular pharmaceutics · 2023Article
- Ambra1 modulates the sensitivity of mantle cell lymphoma to palbociclib by regulating cyclin D1.Scientific reports · 2023Article
- Strategies to Re-Sensitize Castration-Resistant Prostate Cancer to Antiandrogen Therapy.Biomedicines · 2023Review
- MnOMaterials today. Bio · 2023Article
- AMBRA1 and its role as a target for anticancer therapy.Frontiers in oncology · 2022Review
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Androgen deprivation therapy (ADT) is a gold standard treatment for advanced PCa. However, most patients eventually develop the castration-resistant prostate cancer (CRPC) that progresses rapidly despite ongoing systemic androgen deprivation. While early studies indicated that high physiological doses of androgens might suppress rather than promote PCa cell growth in some selective CRPC patients, the exact mechanism of this opposite effect remains unclear. Here we found that Enzalutamide-resistant (EnzR) CRPC cells can be suppressed by the high-dose-androgen (dihydrotestosterone, DHT). Mechanism dissection suggested that a high-dose-DHT can suppress the circular RNA-BCL2 (circRNA-BCL2) expression via transcriptional regulation of its host gene BCL2. The suppressed circRNA-BCL2 can then alter the expression of miRNA-198 to modulate the AMBRA1 expression via direct binding to the 3'UTR of AMBRA1 mRNA. The consequences of high-dose-DHT suppressed circRNA-BCL2/miRNA-198/AMBRA1 signaling likely result in induction of the autophagic cell death to suppress the EnzR CRPC cell growth. Preclinical studies using in vivo xenograft mouse models also demonstrated that AMBRA1-shRNA to suppress the autophagic cell death can weaken the effect of high-dose-DHT on EnzR CRPC tumors. Together, these in vitro and in vivo data provide new insights for understanding the mechanisms underlying high-dose-DHT suppression of the EnzR CRPC cell growth, supporting a potential therapy using high-dose-androgens to suppress CRPC progression in the future.
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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.