Integrative Network Pharmacology and Molecular Docking Reveal the Mechanism of Myricetin in Targeting Key Proteins for Lung Cancer Therapy

Lung cancer is one of the most prevalent types of cancer. Although current treatments such as immunotherapy, targeted therapy, and chemotherapy provide clinical benefits, they are often associated with serious side effects, including drug resistance. Myricetin has demonstrated promising anticancer properties; however, its underlying biological mechanisms and gene interaction networks related to patient survival remain insufficiently explored. This study employs a network pharmacology approach to investigate the interaction network between myricetin and lung cancer–related targets, followed by molecular docking for validation. The analysis revealed 101 nodes and 207 edges within the protein-protein interaction (PPI) network. Centrality analysis identified six key target proteins, and subsequent KEGG pathway enrichment narrowed these to five key proteins, HSP90AA1, CYP19A1, MAPK14, SRC, and AKR1C3, which are involved in seven critical pathways associated with lung cancer progression. Molecular docking demonstrated that myricetin exhibits stronger binding affinities compared to Gefitinib across all targets, with the most favorable binding energy observed with AKR1C3 (-10.6 kcal/mol) and Gefitinib to AKR1C3 (-9.3 kcal/mol). These findings suggest that myricetin exerts multifaceted anticancer effects by modulating key biological processes, including cell proliferation, angiogenesis, inflammation, oxidative stress, and hormonal signaling. Thus, myricetin has the potential to be developed as a therapeutic agent for lung cancer. Therefore, further in vitro analyses are required to evaluate myricetin's anticancer activity in lung cancer cells, along with gene expression studies and safety assessments in normal cells.