ArticleAnimal models and experimental medicine2026
Molecular mechanism of Xanthotoxol against gastric cancer: A comprehensive study integrating network pharmacology, computer simulations, and experimental validation.
Article in Animal models and experimental medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundGastric cancer (GC) is a prevalent malignant tumor of the digestive system worldwide. Xanthotoxol (Xan), a natural compound extracted from traditional Chinese medicine such as Angelica archangelica, has demonstrated antitumor properties. However, its specific effects on GC remain unreported.
methodsHub targets of Xan in GC were identified by integrating weighted gene co-expression network analysis (WGCNA) with network pharmacology. Molecular docking and molecular dynamics (MD) simulations were conducted to analyze the interaction between the hub targets and Xan. The effects of Xan on GC cell proliferation, cell cycle, apoptosis, migration, and invasion were examined using cell experiments and xenograft tumor model. Histopathological evaluation of changes in tumor and liver tissues was performed after Xan intervention. Western blot and reverse transcription quantitative polymerase chain reaction (RT-qPCR) were employed to analyze hub target expression and clarify Xan's molecular mechanism against GC.
resultsA total of six hub genes highly correlated with GC were identified (MMP12, KDR, CCND1, PDGFRB, PLAU, and PLK1). Molecular docking and MD simulations revealed a significant binding affinity between Xan and hub genes. Experiments demonstrated that Xan inhibited proliferation, cell cycle, migration, and invasion while promoting apoptosis. Xan could alleviate liver injury caused by subcutaneous tumor in mice. Furthermore, Xan upregulated MMP12 expression and downregulated KDR, CCND1, PDGFRB, PLAU, and PLK1 in GC cells.
conclusionsXan shows promise as a GC treatment by modulating MMP12, KDR, CCND1, PDGFRB, PLAU, and PLK1 expression, which inhibits proliferation, cell cycle, migration, and invasion, while enhancing apoptosis and reducing liver damage.
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