In vivo (Athens, Greece) · 2026
Magnolol Potentiates Sorafenib-induced Apoptosis and Inhibits Metastatic Signaling in Renal Carcinoma.
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Chang Che-Cheng, Hung Man-Yun, Weng Yueh-Shan, Chang Chieh-Min, Hsu Fei-Ting, Chen Yu-Hsiang, Chen Jiann-Hwa
Аннотация
BACKGROUND/AIM: Sorafenib 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 METHODS: Cell 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.
RESULTS: Combination 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.
CONCLUSION: Magnolol enhances sorafenib efficacy by promoting apoptosis and inhibiting survival and metastatic signaling pathways in renal carcinoma cells.
MATERIALS AND METHODS: Cell 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.
RESULTS: Combination 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.
CONCLUSION: Magnolol enhances sorafenib efficacy by promoting apoptosis and inhibiting survival and metastatic signaling pathways in renal carcinoma cells.
Предметные рубрики MeSH
LignansSorafenibApoptosisSignal TransductionBiphenyl CompoundsAnimalsCell Line, TumorHumansDrug SynergismCell SurvivalCarcinoma, Renal CellKidney NeoplasmsMiceCell MovementProto-Oncogene MasEpithelial-Mesenchymal TransitionNiacinamideCell ProliferationNF-kappa BNeoplasm MetastasisPhenylurea CompoundsErbB ReceptorsAntineoplastic Agents