Abstract
Epigallocatechin-3-gallate (EGCG), the predominant bioactive compound in green tea, has shown promise in lung cancer treatment; however, its molecular targets and antitumor mechanisms remain unclear. In this study, the therapeutic potential of EGCG against non-small cell lung (NSCLC) was evaluated, core targets were prioritized via network pharmacology, and molecular docking were employed to decipher the potential mechanism of action. Using bioinformatics, molecular docking, and functional enrichment analyses, 224 NSCLC-related targets were identified, with TP53, STAT3, AKT1, IL6, HSP90AA1, and JUN emerging as central hubs. Kyoto Encyclopedia of Genes and Genomes (KEGG) and Gene Ontology (GO) analyses revealed oxidative stress regulation and the PI3K/Akt pathway as critical mechanisms. Molecular docking confirmed strong binding affinities between EGCG and hub targets. These findings highlight EGCG as a multi-target agent against NSCLC via PI3K/Akt modulation, redox homeostasis restoration, and inflammation suppression, offering novel insights for phytochemical-based NSCLC therapy.