ArticleOncology letters2026
Jaceosidin inhibits cell viability and induces apoptosis in non-small cell lung cancer by inhibiting the Ras/Raf/MEK/ERK and Akt pathways.
Article in Oncology letters, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Non-small cell lung cancer (NSCLC) remains a major health challenge due to its poor prognosis and low 5-year survival rate; therefore, the development of efficient and less toxic anti-NSCLC therapies is of great importance. The present study aimed to investigate the anti-survival and pro-apoptotic effects of Jaceosidin, a flavonoid, on human NSCLC cells and to uncover its underlying mechanism. Cell viability, cell cycle progression and apoptosis were assess using the MTS assay and flow cytometry, and protein expression was analyzed by western blot analysis. The results showed that Jaceosidin significantly reduced A549 cell viability in a dose-dependent manner, whereas it exhibited significantly lower cytotoxicity against 293T cells. In addition, cell cycle distribution analysis demonstrated that A549 cell treatment with Jaceosidin induced S-phase cell cycle arrest, which was accompanied by p21 upregulation. Jaceosidin also enhanced cell apoptosis, and upregulated cleaved-poly-ADP ribose polymerase and cleaved-caspase-3 expression in a dose-dependent manner. Furthermore, Jaceosidin promoted the release of cytochrome
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