ArticleFrontiers in pharmacology2026
Cyclovirobuxine D suppresses cancer stemness in osteosarcoma with implication of the noncanonical NF-kappaB pathway.
Article in Frontiers in 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
Background: Cyclovirobuxine D (CVB-D), an alkaloid from Buxus microphylla, exhibits anticancer effects in various tumors, but its role in osteosarcoma remains unexplored. This study investigates its efficacy and mechanism in osteosarcoma. Methods: We screened a drug library and evaluated CVB-D's effects on osteosarcoma cell lines using CCK-8 and colony formation assays. Saos2 and K7M2 cells were selected for further analysis. Flow cytometry assessed apoptosis and cell cycle. RNA-seq identified downstream pathways, including NF-kappaB, and stemness markers (CD24, ALDH1A1). Stemness was examined via serum-free suspension culture, and NF-kappaB pathway activator Diprovocim was used in rescue experiments. A xenograft mouse model validated the findings. Results: CVB-D suppressed proliferation, stemness, and induced apoptosis in osteosarcoma. These effects may be partially mediated through the p-NF-kappaB2/NF-kappaB2 axis and were reversible upon NF-kappaB pathway activation. Conclusion: CVB-D inhibits osteosarcoma possibly via the non-canonical NF-kappaB pathway, suggesting a potential therapeutic strategy.
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