ArticleNaunyn-Schmiedeberg's archives of pharmacology2026
Ginsenoside compound K inhibits migration and invasion of melanoma cells by regulating EMT via the IL-6/STAT3 signaling pathway.
Article in Naunyn-Schmiedeberg's archives of pharmacology, 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
The present study aims to investigate the inhibitory effects of ginsenoside compound K (GCK) on malignant melanoma (MM) metastasis and systematically elucidate the underlying molecular mechanisms. Herein, GCK inhibited proliferation, migration, and invasion while promoting apoptosis in MM cells as determined by cell counting kit-8 (CCK-8) assay, Annexin V-FITC/PI apoptosis detection kit, wound-healing, and transwell assay, respectively. Network pharmacology and molecular docking were utilized to identify candidate targets and signaling pathways, which were further confirmed by western blotting and quantitative real-time polymerase chain reaction (qRT-PCR). To validate the mechanistic involvement of the IL-6/STAT3 signaling pathway, rescue experiments were performed using IL-6-overexpressing A375 cells, and the in vivo antitumor efficacy of GCK was evaluated in a B16F10 melanoma xenograft model in C57BL/6J mice. In vitro cytotoxicity assays demonstrated that GCK exerted potent cytotoxic effects against A375 cells, with an IC
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