International dental journal · 2026
Exploring the Mechanism of Oral Cancer With Shikonin Based on the Network Pharmacology and Molecular Docking Technology.
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Hou Lin, Wang Kun, Wang Yusheng, Li Jing, Guo Lin, Zhao Qingliang
Аннотация
OBJECTIVES: To explore the underlying mechanisms of shikonin in treating oral cancer using network pharmacology and molecular docking methods.
MATERIALS AND METHODS: Targets of shikonin were obtained from the TCMSP, BATMAN, ChEMBL, PharmMapper and HERB databases. Targets of oral cancer were gathered from the OMIM, STITCH, GeneCards and Drugbank databases. The intersection targets of shikonin and oral cancer were obtained for subsequent analysis. The intersecting targets of shikonin and oral cancer were entered into the DAVID database and used its functions to perform Gene Ontology (GO) and Kyoto encyclopaedia of genes and genomes (KEGG) enrichment analysis on the intersection targets to obtain the relevant pathways and biological functions of shikonin in the treatment of oral cancer. The protein-protein interaction (PPI) network of shikonin and oral cancer targets was constructed in STRING platform. Subsequently, using Cytoscape 3.8.0 to obtain the key targets of shikonin and oral cancer. Finally, molecular docking and molecular dynamics simulations were used to evaluate the strength of binding between shikonin and key targets, as well as the hydrogen bonds involved.
RESULTS: In total, 481 targets were screened for shikonin, and 10,058 targets were identified for oral cancer. By GO and KEGG analysis, the targets of shikonin and oral cancer may be involved in the mediation of apoptosis, inflammation and immune response. And the associated signalling pathways that targets may be involved in the treatment of oral cancer, including the FoxO signalling pathway, HIF-1 signalling pathway, TNF signalling pathway, and Th17 cell differentiation, etc. Cytoscape software screened the key genes including AKT1, MAPK1, CXCR4, CXCL8, CCL3, CCL4, CCL5, CYBB, BCL2, NOX1, HIF-1, TP53. The results of molecular docking and molecular dynamics simulations showed that shikonin exhibits good binding interactions with CCL3, AKT1 and NOX1.
CONCLUSIONS: Mulitple molecular mechanisms involved in oral cancer management with shikonin have been elucidated providing a glimpse og the underlying therapeutic targets for the disease.
MATERIALS AND METHODS: Targets of shikonin were obtained from the TCMSP, BATMAN, ChEMBL, PharmMapper and HERB databases. Targets of oral cancer were gathered from the OMIM, STITCH, GeneCards and Drugbank databases. The intersection targets of shikonin and oral cancer were obtained for subsequent analysis. The intersecting targets of shikonin and oral cancer were entered into the DAVID database and used its functions to perform Gene Ontology (GO) and Kyoto encyclopaedia of genes and genomes (KEGG) enrichment analysis on the intersection targets to obtain the relevant pathways and biological functions of shikonin in the treatment of oral cancer. The protein-protein interaction (PPI) network of shikonin and oral cancer targets was constructed in STRING platform. Subsequently, using Cytoscape 3.8.0 to obtain the key targets of shikonin and oral cancer. Finally, molecular docking and molecular dynamics simulations were used to evaluate the strength of binding between shikonin and key targets, as well as the hydrogen bonds involved.
RESULTS: In total, 481 targets were screened for shikonin, and 10,058 targets were identified for oral cancer. By GO and KEGG analysis, the targets of shikonin and oral cancer may be involved in the mediation of apoptosis, inflammation and immune response. And the associated signalling pathways that targets may be involved in the treatment of oral cancer, including the FoxO signalling pathway, HIF-1 signalling pathway, TNF signalling pathway, and Th17 cell differentiation, etc. Cytoscape software screened the key genes including AKT1, MAPK1, CXCR4, CXCL8, CCL3, CCL4, CCL5, CYBB, BCL2, NOX1, HIF-1, TP53. The results of molecular docking and molecular dynamics simulations showed that shikonin exhibits good binding interactions with CCL3, AKT1 and NOX1.
CONCLUSIONS: Mulitple molecular mechanisms involved in oral cancer management with shikonin have been elucidated providing a glimpse og the underlying therapeutic targets for the disease.