ArticleBMC cancer2025
Combining network pharmacology and experimental verification to explore the inhibitory effects of Deoxyelephantopin (DET) Against Non-Small Cell Lung Cancer (NSCLC).
Article in BMC cancer, 2025. 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
backgroundDET has a significant inhibitory activity against a range of cancer cells; however, its specific effects and underlying mechanisms in Non-Small Cell Lung Cancer (NSCLC) remain to be fully elucidated. This study aimed to investigate the potential mechanisms through which DET exerts its anti-neoplastic effects on NSCLC.
methodTargets of DET were predicted using the SwissTargetPrediction database. Disease targets for NSCLC were obtained from the GeneCards database, and the intersection between drug targets and disease targets was determined. The STRING database was then employed to construct a protein-protein interaction (PPI) network and analyze target interactions. Additionally, Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG)enrichment analyses were conducted to investigate their biological functions. Molecular docking simulations were conducted using AutoDock software to analyze the binding interactions between DET and key target proteins. Subsequently, both in vitro and in vivo experiments were carried out to evaluate the anticancer effects of DET, with alterations in key gene expression levels assessed through RT-qPCR and Western blot analyses.
resultsA total of 52 potential targets were discovered for DET and NSCLC. The PPI analysis revealed 5 hub targets, including CASP3, PTGS2, TNFα, ICAM1 and JUN. GO analysis identified 164 biological processes, 44 molecular functions and 40 cellular components. KEGG analysis revealed that DET anticancer effects were mediated through multiple pathways, primarily the AGE-RAGE and TNF signaling pathways. Experimental results demonstrated that DET inhibited the proliferation and migration of H460 cells and induced apoptosis in vitro. RT-qPCR and WB indicated that DET up regulated Bax and CASP3 while down regulating Bcl2, JUN, TNFα, NF-κB, ICAM1 and PTGS2.
conclusionThis study aims to investigate the inhibitory effect of DET on NSCLC by combining network pharmacology and experimental methods. The results demonstrate that DET effectively inhibited the proliferation of H460 cells and induced apoptosis, with significant involvement of the AGE-RAGE and TNF signaling pathways, suggesting its potential as a therapeutic intervention for NSCLC.
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