Byakangelicin suppresses renal cell carcinoma progression via modulation of Wnt/β-catenin signaling pathway

AimTo explore the impact of the active ingredient Byakangelicin (BYA) from Angelica dahurica on the biological behavior of renal cell carcinoma cells and its potential mechanisms of action.MethodsThe active components of Angelica dahurica and their target genes were screened via network pharmacology. RCC-related targets were retrieved from OMIM, GeneCards, Disgenet, CTD, and NCBI data-bases. A "drug-component-target-disease" network was constructed using Cytoscape, and a PPI network was built via STRING. GO and KEGG analyses were performed using DAVID. The effects of BYA on RCC cell growth, migration, and invasion were validated through in vitro experiments. The binding energy of Byakangelicin to GSK-3β was analyzed using via molecular docking.ResultsThe study identified 11 active compounds with significant efficacy, sharing 10 common targets with RCC. Target proteins were primarily enriched in cancer-related pathways, including the PI3K/AKT signaling pathway and proteoglycans in cancer pathway. In vitro cell experiments demonstrated that BYA significantly inhibited the proliferation, migration and invasion of RCC cells, and induced cell cycle arrest at the S phase. Additionally, the inhibitory effects of BYA could be reversed by an agonist of the Wnt/β-Catenin signaling pathway.ConclusionBYA inhibits the proliferation, migration and invasion of RCC cells by regulating the Wnt/β-catenin signaling pathway, while inducing cell cycle arrest at the S-phase.