ArticleEndocrine, metabolic & immune disorders drug targets2024
Network Pharmacological Analysis and Experimental Validation of the Effects of Silybin on Proliferation, Migration, and Immunotherapy of Papillary Thyroid Cancer.
Article in Endocrine, metabolic & immune disorders drug targets, 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, 5 citations in OpenAlex.
- Natural Compounds Targeting MAPK, PI3K/Akt, and JAK/STAT Signaling in Papillary Thyroid Cancer.International journal of molecular sciences · 2025Review
- Natural anti-cancer products: insights from herbal medicine.Chinese medicine · 2025Review
- Elucidation of the mechanism Underlying the promotion of ferroptosis and enhanced antitumor immunity by citrus polymethoxyflavones in CRC cells.Frontiers in pharmacology · 2025Article
- The regulatory network of epithelial-mesenchymal transition-associated non-coding RNAs in thyroid cancer: molecular mechanisms, clinical implications, and therapeutic strategies.Frontiers in oncology · 2025Review
- Advances in PD-1/PD-L1 pathway inhibitors in the treatment of thyroid cancer: mechanisms and clinical therapeutic perspectives.Frontiers in immunology · 2025Review
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimThe study aimed to use network pharmacology research and
backgroundPapillary thyroid cancer (PTC) has a decent prognosis; however, recurrence and metastasis are the leading causes of death in patients with PTC. A key research focus in thyroid cancer treatment is the inhibition of PTC proliferation, invasion, and migration. Silybin, the major active element in the traditional Chinese herb silymarin, has been used to treat a range of diseases, including cancer, but no study has been undertaken to determine whether it can help prevent PTC.
objectiveIn this study, we attempted to determine through network pharmacology and
methodsTo predict the probable targets and underlying mechanisms of silybin against PTC, a network pharmacology research was performed.
resultsThe datasets revealed a total of 489 silybin targets acting on PTC, and functional enrichment analysis suggested that the target genes were enriched in functions and pathways related to PTC development, invasion, migration, and immunotherapy. By constructing these target PPI networks, the seven hub genes, fibronectin 1 (FN1), tissue inhibitor of metalloproteinases 1 (TIMP1), N-cadherin (CDH2), collagen type III alpha 1 chain (COL3A1), cyclin D1 (CCND1), AP-1 transcription factor subunit (JUN), and hepatocyte growth factor receptor (MET) were found. These hub genes were determined to be highly linked to a worse clinicopathological form, a higher risk of metastatic recurrence, and a worse prognosis of PTC. The common immunological checkpoint gene expression levels were positively correlated with the expression levels of the hub genes. Silybin decreased the proliferative and metastatic capacity of PTC cells, according to
conclusionThese findings provide preliminary evidence that silybin inhibits PTC cell proliferation, metastasis, and invasion by altering the FN1/AKT signaling pathway and inhibiting the EMT process. Silybin can reverse immunosuppression in papillary thyroid cancer by affecting immunological checkpoint gene expression levels. These studies provide a theoretical and experimental scientific basis for the potential anticancer effects of silybin on PTC.
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