Using network pharmacological analysis and molecular docking to investigate the mechanism of action of quercetin's suppression of oral cancer.

Abstract

This investigation seeks to explore the mechanism of quercetin in oral cancer by incorporating network pharmacology analysis and molecular docking. First, we use the network pharmacology analysis to discover possible core targets for quercetin and oral cancer. We subsequently utilized the docking of molecules techniques to calculate the affinities of critical targets and quercetin for verification. TCMSP and the Swiss Target Prediction database found 190 quercetin action targets, while GeneCards, OMIM, PharmGkb, and the Therapeutic Target Database found 8971 oral cancer-related targets. Venny 2.1.0 online software conducted an intersection analysis of quercetin-related target information with information about oral cancer, and 172 putative quercetin-anti-oral cancer targets were examined. Six prospective core targets for quercetin treatment of oral cancer were identified from the PPI network topology analysis of 172 putative therapeutic targets. These targets include AKT1, PIK3R1, MYC, HIF1A, SRC, and HSP90AA1. GO enrichment function analysis showed that 2372 biological processes, 98 cell components, and 201 molecular functions were involved. Through enrichment analysis of the KEGG pathway, 172 signal pathways were obtained. A few examples are PI3K-AKT, HIF-1, IL-17, and other signaling pathways. The molecular docking scores of quercetin and the primary therapeutic targets AKT1, HIF1A, HSP90AA1, MYC, PIK3R1, and SRC are all less than -0.7 points, demonstrating good compatibility between the medicine and small molecules and suggesting that quercetin may affect oral cancer through the primary target. This study explores quercetin's mechanism and possible targets for oral cancer treatment, offering novel approaches. Quercetin may be a multitarget medication against oral cancer in the future.