Research on the mechanism of gastrodin in the treatment of liver cancer based on network pharmacology
Objective: Liver cancer remains a major cause of cancer mortality, with rising incidence worldwide. Gastrodin, a bioactive compound from Gastrodia elata, has shown anti-cancer potential. This study applied bioinformatics analyses to identify liver-specific pharmacological targets of gastrodin, examining their roles in liver cancer. Methods: Data on normal liver tissue, liver cancer, and gastrodin were retrieved from multiple databases, including GeneCards, Herb, and TCMSP. These datasets were analyzed using Venny, InteractiVenn, and MetaScape for integrative analysis and visualization. MetaScape was used for enrichment analysis and protein–protein interaction (PPI) network construction, while Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways, and Cytoscape facilitated detailed functional and network visualization. Results: Intersected genes among liver tissue, liver cancer, and gastrodin were identified via Venn analysis. The key targets were obtained, including glucokinase (GCK), insulin receptor (INSR), hexokinase 1 (HK1), glucosamine-6-phosphate deaminase 1 (GNPDA1), superoxide dismutase 1 (SOD1), and SNF2 related chromatin remodeling ATPase 5 (SMARCA5), as well as high maximal clique centrality (MCC)-scoring proteins such as glycogen synthase kinase 3 beta (GSK3B), galectin-3L (GALS3), androgen receptor (AR), coagulation factor II, thrombin (F2), and F3. GO and KEGG analyses further demonstrated the therapeutic potential of these key targets in the treatment of liver cancer. Conclusions: This study identified potential pharmacological targets in liver cancer influenced by gastrodin, enhancing understanding of its therapeutic mechanisms and supporting its potential application in liver cancer treatment.
Publication Details
- Journal
- New discovery.
- Published
- 2025-09-20
- DOI
- https://doi.org/10.61958/quba7215
- Primary Topic
- Neuroinflammation and Neurodegeneration Mechanisms
- Type
- article
- Field-Weighted Citation Impact
- 0.00