ArticleIn vivo (Athens, Greece)
Magnolol Potentiates Sorafenib-induced Apoptosis and Inhibits Metastatic Signaling in Renal Carcinoma.
Article in In vivo (Athens, Greece). 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
BACKGROUND/
aimSorafenib is a standard targeted therapy for renal cell carcinoma; however, resistance and limited efficacy remain clinical challenges. Magnolol, a bioactive compound derived from Magnolia officinalis, exhibits anti-cancer properties, and may enhance therapeutic responses. This study investigated whether magnolol potentiates the anti-tumor effects of sorafenib in murine renal carcinoma (Renca) cells and explored the underlying molecular mechanisms. MATERIALS AND
methodsCell viability was assessed by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, and drug interactions were analyzed using the Chou-Talalay method. Apoptosis was evaluated by Annexin V/propidium iodide (PI) staining, cell-cycle analysis, and caspase activation. Western blotting and flow cytometry were performed to examine apoptotic pathways and epidermal growth factor receptor (EGFR)/SRC proto-oncogene, non-receptor tyrosine kinase (SRC)/nuclear factor kappa B (NF-κB) signaling. Transwell assays and protein expression profiling were used to analyze migration, invasion, and epithelial-mesenchymal transition (EMT) markers.
resultsCombination treatment synergistically reduced cell viability, with a combination index (CI) <1, and significantly enhanced apoptosis via activation of intrinsic and extrinsic pathways. Co-treatment suppressed EGFR/SRC proto-oncogene, SRC/ NF-κB signaling and reduced migration, invasion, and EMT-associated markers.
conclusionMagnolol enhances sorafenib efficacy by promoting apoptosis and inhibiting survival and metastatic signaling pathways in renal carcinoma cells.
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