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Background <p>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.</p> Objective <p>To identify potential molecular targets of luteolin in pancreatic cancer and elucidate the underlying therapeutic mechanisms through comprehensive bioinformatics and experimental approaches.</p> Methods <p>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.</p> Results <p>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 (−&#xa0;8.0&#xa0;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.</p> Conclusion <p>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.</p>

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

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年3月9日

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  • Danhong Pan,
  • Shixia Li,
  • Peixi Zhong,
  • Lili Chen,
  • Binbo Fang,
  • Yifu Feng

摘要

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.