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Network pharmacology of Sijunzi decoction in pancreatic cancer
Rujia Zheng1, Qitai Chen1, Mengting Zhang2
1MOE Joint International Research Laboratory of Pancreatic Diseases, Department of Hepatobiliary and Pancreatic Surgery, The First Affiliated Hospital of Zhejiang University School of Medicine, Hangzhou, China.
Background:
Sijunzi decoction (SJZD) is a traditional Chinese medicine (TCM) commonly used for pancreatic ductal adenocarcinoma (PDAC), but its mechanisms remain unclear. This study investigates its molecular basis using network pharmacology and molecular docking.
Methods:
Active compounds and targets of SJZD were identified via Traditional Chinese Medicine Systems Pharmacology (TCMSP) Database and Analysis Platform, and PDAC-related targets were retrieved from Online Mendelian Inheritance in Man (OMIM) and GeneCards. Protein-protein interaction (PPI) networks, Gene Ontology (GO)/Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment, and tissue distribution analyses were conducted. Molecular docking evaluated binding affinities between compounds and targets. The anti-PDAC effects of SJZD were evaluated in vitro using human pancreatic cancer cell lines (CFPAC-1 and MiaPaCa-2) and in vivo using a patient-derived xenograft (PDX) mouse model.
Results:
SJZD comprises 131 compounds and 260 targets, with key targets such as AKT serine/threonine kinase 1 (AKT1), BCL2 associated agonist of cell death (BAD), BCL2 apoptosis regulator (BCL2), and tumor protein p53 (TP53) identified through PPI analysis. Enrichment analyses highlighted the phosphatidylinositide 3-kinases (PI3K)/protein Kinase B (AKT)/mechanistic target of rapamycin kinase (mTOR) and apoptosis pathways as primary therapeutic mechanisms. SJZD exhibited cytotoxic effects against PDAC cells in vitro and suppressed tumor growth in vivo, with mechanistic analyses confirming its regulatory effects on the PI3K/AKT/mTOR and apoptosis pathways. Molecular docking revealed strong binding affinities, particularly for compounds targeting estrogen receptor 1 (ESR1) and estrogen receptor 2 (ESR2). These findings suggest that SJZD exerts anti-PDAC effects via multi-target modulation, primarily through inhibition of the PI3K/AKT/mTOR signaling axis, induction of apoptosis and autophagy, and anti-inflammatory activity. The involvement of classic compounds supports the rationale of its traditional use, while experimental validation provides a mechanistic foundation for future clinical development.
Conclusions:
This study clarifies the active components, targets, and mechanisms of SJZD in treating PDAC, offering insights into the therapeutic potential of TCM.