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<p>Head and neck squamous cell carcinoma (HNSCC) exhibits a poor prognosis, with 5-year survival rates below 50%. This study employed network pharmacology to investigate the anti-HNSCC mechanism of silibinin, a plant-derived compound with established anticancer activity. We obtained potential silibinin targets from pharmacological databases and HNSCC-associated targets from TCGA. We performed Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses to identify critical pathways and biological processes. Through protein–protein interaction (PPI) network screening, we selected hub genes for molecular docking validation. We evaluated silibinin’s effects on HNSCC proliferation and invasion using CCK-8 assays, colony formation tests, and cell invasion experiments. Our data suggested that silibinin may inhibit HNSCC progression through modulation of the interleukin-17 signaling pathway. Molecular docking confirmed strong binding affinity between silibinin and key targets, supporting its potential as an HNSCC therapeutic agent.</p>

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Unveiling the therapeutic potential of silibinin in head and neck squamous cell carcinoma via network pharmacology

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年11月20日

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  • Yu Zheng,
  • You Xia,
  • Junjun Ling,
  • Houyu Zhao,
  • Xianlu Zhuo

摘要

Head and neck squamous cell carcinoma (HNSCC) exhibits a poor prognosis, with 5-year survival rates below 50%. This study employed network pharmacology to investigate the anti-HNSCC mechanism of silibinin, a plant-derived compound with established anticancer activity. We obtained potential silibinin targets from pharmacological databases and HNSCC-associated targets from TCGA. We performed Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses to identify critical pathways and biological processes. Through protein–protein interaction (PPI) network screening, we selected hub genes for molecular docking validation. We evaluated silibinin’s effects on HNSCC proliferation and invasion using CCK-8 assays, colony formation tests, and cell invasion experiments. Our data suggested that silibinin may inhibit HNSCC progression through modulation of the interleukin-17 signaling pathway. Molecular docking confirmed strong binding affinity between silibinin and key targets, supporting its potential as an HNSCC therapeutic agent.