ArticleNaunyn-Schmiedeberg's archives of pharmacology2025
Exploring the mechanisms of cinobufotalin in ovarian cancer treatment: An integrated approach combining network pharmacology, molecular docking and RNA Sequencing.
Article in Naunyn-Schmiedeberg's archives of pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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4 authors.
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Abstract
Cinobufotalin (CINO), a bioactive compound derived from toad skin secretions, has demonstrated clinical efficacy in cancer treatment. However, its molecular mechanisms in ovarian cancer (OC) remain poorly characterized. This study systematically investigated the anti-OC mechanisms of CINO through an integrated strategy combining network pharmacology, molecular docking, and RNA sequencing. Potential CINO targets were predicted via Swiss Target Prediction, while OC-related genes were retrieved from GeneCards and OMIM. Intersecting targets were analyzed using PPI networks and functional enrichment (GO/KEGG). Molecular docking validated ligand-target interactions, and RNA-seq quantified differential gene expression in CINO-treated SKOV3 cells. Among 69 overlapping targets, 10 hub genes (EGFR, PTGS2, MDM2, MAPK1, MAPK3, MTOR, ESR1, PIK3CA, MMP9, and GSK3B) were identified. KEGG analysis highlighted the MAPK signaling and endocrine resistance pathways. RNA-seq revealed 1488 upregulated and 3253 downregulated DEGs, which were mainly enriched in axon development, axonogenesis, and primarily involved in the MAPK signaling pathway. CINO significantly suppressed EGFR, ESR1, MAPK1, MDM2, and mTOR expression (p < 0.05), aligning with pathway predictions. CINO exerts anti-OC effects by modulating endocrine resistance and MAPK signaling, providing a mechanistic foundation for its clinical application.
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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.