2. Academic Validation
  3. Integrative analysis reveals luteolin's molecular targets and mechanisms in pancreatic cancer treatment

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

  • Eur J Med Res. 2026 Mar 9. doi: 10.1186/s40001-026-04056-x.
Danhong Pan 1,  Shixia Li 2,  Peixi Zhong 2,  Lili Chen 1,  Binbo Fang 3 4,  Yifu Feng 5
Affiliations

Affiliations

  • 1 Department of EICU, The First People's Hospital of Wenling (Taizhou University Affiliated Wenling Hospital), School of Medicine, Taizhou University, Zhejiang, 317500, Wenling, China.
  • 2 Department of Clinical Medicine, School of Medicine, Taizhou University, Taizhou, 318000, Zhejiang, China.
  • 3 Department of Clinical Medicine, School of Medicine, Taizhou University, Taizhou, 318000, Zhejiang, China. [email protected].
  • 4 Department of Medicine, Taizhou University, 1139 Shifu Avenue, Jiaqian Street, Jiaojiang District, Taizhou, Zhejiang, People's Republic of China. [email protected].
  • 5 Department of Hepatobiliary Surgery, Taizhou Central Hospital (Taizhou University Hospital), School of Medicine, Taizhou University, No. 999 Donghai Avenue, Jiaojiang Economic Development Zone, Taizhou, Zhejiang, People's Republic of China. [email protected].
PMID: 41803987 DOI: 10.1186/s40001-026-04056-x
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.

Keywords

Luteolin; MET; Network pharmacology; PI3K/AKT; Pancreatic cancer.

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