ArticleFrontiers in molecular biosciences2025
Integrating network pharmacology and experimental validation to reveal the anti-growth mechanism of panaxadiol against glioblastoma via calcium signaling.
Article in Frontiers in molecular biosciences, 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
Glioblastoma (GBM) is a highly aggressive brain tumor and is relatively common among malignant brain tumors in adults. Its rapid proliferation and significant invasiveness make its treatment one of the major challenges in brain tumor research. Panaxadiol, a compound extracted from ginseng roots, has been found to have significant therapeutic effects on various types of tumors. Nonetheless, the precise function and underlying mechanisms of this factor in GBM have yet to be thoroughly investigated. In the current study, we employed network pharmacology to explore the potential therapeutic interactions of Panaxadiol within the framework of GBM. Subsequently, we confirmed its efficacy via biological experiments aimed at elucidating the mechanisms through which it exerts its anti-GBM effects. We collected relevant targets of Panaxadiol and differential genes of GBM from multiple databases. The network pharmacology analysis revealed 66 potential targets of Panaxadiol in the context of GBM. Enrichment analysis indicated that these targets might function through several key signaling pathways, including the calcium, cAMP, and cGMP-PKG signaling pathways. Therefore, Panaxadiol may exert its effects by regulating calcium ions. Further, In our study, we employed the MOCDE and CytoHubba plugins within the Cytoscape framework to identify seven hub genes, including GRIA2, GRIN1, GRIN2B, GRM1, GRM5, HTR1A, and HTR2A, and validated their binding capabilities with Panaxadiol through molecular docking. Furthermore, we conducted experiments
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