Integrating network pharmacology, molecular docking, and experimental verification to investigate the mechanism of baicalein in colorectal cancer.

Background: Baicalein (BA) is a major bioactive flavonoid derived from Methods: First, potential targets of BA and CRC were retrieved from public databases, and overlapping targets were identified. A protein-protein interaction (PPI) network was established, and candidate targets were analyzed using Gene Ontology (GO), Disease Ontology (DO), and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses to identify signaling pathways through which BA may exert therapeutic effects in CRC. The stability of ligand-receptor binding was evaluated via molecular docking and MDS. Finally, the identified core targets and associated signaling pathways were validated through Results: NP analysis identified 171 overlapping targets between CRC and BA, with EGFR, AKT1, MAPK3 (ERK1), BCL2, GSK3B, and SRC identified as the core nodes. Molecular docking and MDS revealed that BA forms stable interactions with the kinase domain of EGFR. Integrated enrichment analysis and Conclusions: BA inhibits CRC progression by inhibiting EGFR activation and modulating MAPK and PI3K/AKT signaling pathways. These findings provide a theoretical basis for developing BA as a natural therapeutic agent for CRC treatment.