ArticleOncogene2025
Increased antiandrogen enzalutamide sensitivity via altering prostate cancer stem cell traits through modulating the androgen receptor-mediated CDR1/circCDR1-AS/miR-1290/BMP4 signaling.
Article in Oncogene, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
- Matrix Stiffness Directs Stemness Signatures in Breast Cancer.Advanced healthcare materials · 2026Article
- Unravelling therapeutic resistance: role of cancer stem cell and microRNA in metastatic prostate cancer.Frontiers in molecular biosciences · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
17 authors.
Funding
Abstract
While the recent FDA-approved antiandrogen enzalutamide (Enz) might prolong the survival of castration-resistant prostate cancer (CRPC) patients by an additional 4.8 months, most patients eventually might still develop Enz resistance within 6-12 months. Although few genes have been linked to Enz resistance in prostate cancer (PCa), the detailed mechanism(s) are still underinvestigated. Here, we found that Enz might function by altering androgen receptor(AR)-mediated CDR1/circCDR1-AS/miR-1290/BMP4 signaling to modulate PCa stem cells (CSCs) to increase Enz resistance. Mechanistic analysis revealed that Enz/AR signaling can transcriptionally regulate CDR1 expression by reducing binding to androgen response elements (AREs) on the CDR1 5' promoter to alter circCDR1-AS expression. Enz/AR/CDR1/circCDR1-AS signaling might then increase BMP4 expression by altering miR-1290 expression, which involves direct binding to the 3' UTR of BMP4 mRNA. Preclinical studies using a CWR22Rv1 xenograft mouse model and integrative analysis of GEO cohort data further demonstrated that targeting this newly identified Enz/AR/CDR1/circCDR1-AS/miR-1290/BMP4 signaling pathway with miR-1290, circCDR1-AS-shRNA, or BMP4-shRNA may help develop novel therapies to combat Enz resistance at the later stage of CRPC.
Indexed as
Identifiers
What OpenQuestion holds
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.