ArticleClinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico2026
Sanguinarine chloride exerts its antitumor effects on enzalutamide-resistant prostate cancer by inhibiting cell proliferation and promoting senescence via targeting AR signaling.
Article in Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors.
Funding
Abstract
objectiveProstate cancer (PCa) remains a leading cause of cancer-associated morbidity among men globally. Although enzalutamide (ENZ), a second-generation androgen receptor (AR) antagonist, serves as a mainstay therapy for castration-resistant prostate cancer (CRPC), therapeutic resistance inevitably emerges. This underscores an urgent demand for innovative treatment strategies.
methodsCCK-8, colony formation, EdU staining, flow cytometry, Hoechst 33,258 staining, western blotting, proteomics analysis, and senescence-associated β-galactosidase (SA-β-gal) staining were performed to reveal the role and underlying mechanisms of S.C in ENZ-resistant prostate cancer. Target prediction, molecular docking, and cellular thermal shift assay (CETSA) were used to identify the target of S.C. Finally, the impact of S.C in vivo was evaluated using ENZ-resistant xenograft models.
resultsOur results showed that S.C effectively suppresses cell viability in ENZ-resistant models through the dual induction of apoptosis and cellular senescence. Database mining, molecular docking, and CETSA identified AR as a putative target of S.C, which was subsequently validated in vivo. S.C treatment significantly inhibited the AR signaling pathway and suppressed tumor growth in ENZ-resistant xenograft models.
conclusionTo our knowledge, this study demonstrates that S.C could be a promising multi-mechanistic agent which can overcome ENZ resistance by targeting AR and inducing two distinct cell death pathways, offering a potential novel therapeutic strategy for CRPC.
Indexed as
Identifiers
42669084What Socratic 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 Socratic graph.