ArticleJournal of pharmacopuncture2025
In Silico Assessment of
Article in Journal of pharmacopuncture, 2025. 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
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objectives: Prostate cancer is a globally prevalent malignancy with rising resistance to conventional therapies. Although awareness and early diagnosis have improved through screening campaigns, there remains a need for alternative strategies. Methods: Core targets related to both SM and prostate cancer were identified through a network pharmacology approach. Protein-protein interaction networks, Gene Ontology (GO), and KEGG enrichment analyses were performed to interpret biological relevance. Molecular docking was used to evaluate the binding affinity of SM's bioactive components with selected targets. Results: Key proteins identified included SRC, PIK3CD, CDK1, CCNA2, PTPN11, PTK2, RXRA, CYP2C9, and PTGS2, showing significant relevance to SM and prostate cancer. GO analysis emphasized "response to organic cyclic compounds" as a significant term. KEGG and GO enrichment analyses indicated that synaptic and neuronal pathways are central in the disease's progression. Docking simulations revealed strong interactions between core targets and SM constituents, notably (+)-silymonin and silandrin. Conclusion: This integrated approach highlighted critical molecular targets and pathways modulated by SM, providing a basis for future experimental studies. SM shows potential as a complementary agent in prostate cancer therapy.
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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.