ArticleBMC urology2024
In silico exploration of anti-prostate cancer compounds from differential expressed genes.
Article in BMC urology, 2024. 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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Who cites it
5 citing papers in PubMed.
- Systems biology-driven drug repurposing in glioblastomaResearch in pharmaceutical sciences · 2026Article
- Chrysin and Luteolin from Moroccan Propolis to Prevent Aggressive Periodontitis Caused byPharmaceuticals (Basel, Switzerland) · 2026Article
- High-throughput screening identifies novel chemical scaffolds targeting Leishmania donovani parasites.World journal of microbiology & biotechnology · 2025Article
- In silico identification of PPARγ agonists from diffractaic acid analogs in prostate cancer: a comprehensive computational approach.3 Biotech · 2025Article
- In silico molecular targets, docking, dynamics simulation and physiologically based pharmacokinetics modeling of oritavancin.BMC pharmacology & toxicology · 2024Article
Corrections and comments
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Authors and funding
8 authors.
Funding
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Abstract
Prostate cancer (PCa) is a complex and biologically diverse disease with no curative treatment options at present. This study aims to utilize computational methods to explore potential anti-PCa compounds based on differentially expressed genes (DEGs), with the goal of identifying novel therapeutic indications or repurposing existing drugs. The methods employed in this study include DEGs-to-drug prediction, pharmacokinetics prediction, target prediction, network analysis, and molecular docking. The findings revealed a total of 79 upregulated DEGs and 110 downregulated DEGs in PCa, which were used to identify drug compounds capable of reversing the dysregulated conditions (dexverapamil, emetine, parthenolide, dobutamine, terfenadine, pimozide, mefloquine, ellipticine, and trifluoperazine) at a threshold probability of 20% on several molecular targets, such as serotonin receptors 2a/2b/2c, HERG protein, adrenergic receptors alpha-1a/2a, dopamine D3 receptor, inducible nitric oxide synthase (iNOS), epidermal growth factor receptor erbB1 (EGFR), tyrosine-protein kinases, and C-C chemokine receptor type 5 (CCR5). Molecular docking analysis revealed that terfenadine binding to inducible nitric oxide synthase (-7.833 kcal.mol
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