Integrative analysis reveals luteolin's molecular targets and mechanisms in pancreatic cancer treatment.

Di Pan, Shih-Wein Li, P Y Zhong, L M Chen, Bing-Hu Fang, Yibin Feng

Eur J Med Res

Mar 9, 2026

Sources

0:00 / 0:00

Sign in to access this feature

Create a free account or sign in to use AI summaries, listen to articles, download PDFs, and save to your library.

137 views

Abstract

BACKGROUND: Pancreatic cancer remains one of the most lethal malignancies with limited therapeutic options. Luteolin, a natural flavonoid compound, has demonstrated potential anti-cancer properties, but its specific mechanisms of action in pancreatic cancer are not fully understood. OBJECTIVE: To identify potential molecular targets of luteolin in pancreatic cancer and elucidate the underlying therapeutic mechanisms through comprehensive bioinformatics and experimental approaches. METHODS: We employed multiple databases including SwissTargetPrediction, GeneCards, and OMIM to predict luteolin targets and pancreatic cancer-related genes. Differential gene expression analysis was performed using the GSE32676 dataset. KEGG and GO enrichment analyses were conducted to identify key pathways. Molecular docking and dynamics simulations validated protein-ligand interactions. TCGA data analysis examined MET expression patterns and prognostic significance. In vitro and in vivo experiments confirmed luteolin's therapeutic effects. RESULTS: We identified 7 overlapping genes between luteolin targets and pancreatic cancer-related genes, with MET emerging as the primary target through network analysis. Molecular docking revealed stable binding between luteolin and MET (- 8.0 kcal/mol). Molecular dynamics simulations confirmed the structural stability of the MET-luteolin complex. TCGA analysis showed MET overexpression in pancreatic cancer correlating with poor prognosis. Experimental validation demonstrated that luteolin inhibited pancreatic cancer cell proliferation and tumor growth through MET/PI3K/AKT pathway modulation. CONCLUSION: This study identifies MET as a critical therapeutic target of luteolin in pancreatic cancer, providing mechanistic insights into luteolin's anti-cancer effects via the MET/PI3K/AKT signaling pathway and supporting its potential clinical application.