ArticleJournal of translational medicine2026
Antitumor effects of Santalol on non-small cell lung cancer via disruption of NF-κB-mediated lipid metabolism.
Article in Journal of translational medicine, 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.
- Green Fabrication and Characterization of Copper Oxide Nanoparticles Using C. Gigantea Leaf Extract and Their ROS-Mediated Anticancer Activity Against A549 Lung Cancer Cells.Cell biochemistry and biophysics · 2026Article
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundNon-small cell lung cancer (NSCLC) poses significant therapeutic challenges, highlighting the urgent need for novel and effective therapeutic strategies. PURPOSE: This study aimed to investigate the antitumor potential of Santalol, a natural compound, in NSCLC and to explore its underlying molecular mechanisms, with a particular focus on lipid metabolism and NF-κB signaling.
methodsThe anti-tumor effects of Santalol were assessed in vitro using NSCLC cell lines (A549, PC9) via proliferation, cell cycle, apoptosis, migration, and invasion assays, along with EMT marker expression. Transcriptomic analysis (RNA sequencing) and functional assays (lipid metabolism, NF-κB phosphorylation) were used to explore molecular mechanisms. In vivo efficacy was evaluated using an A549 xenograft mouse model.
resultsSantalol dose-dependently inhibited NSCLC cell proliferation, induced G1 phase cell cycle arrest and apoptosis, and significantly suppressed migration, invasion, and modulated EMT markers. Transcriptomic and functional analyses revealed that Santalol altered genes associated with lipid metabolism and the NF-κB pathway. Specifically, Santalol reduced fatty acid synthase (FASN) activity, decreased intracellular free fatty acid levels, and inhibited NF-κB phosphorylation. In vivo, Santalol markedly suppressed tumor growth and reduced Ki67 expression without observable systemic toxicity.
conclusionSantalol exerts robust anti-NSCLC effects by inhibiting proliferation, migration, and invasion. These effects are mechanistically associated with the modulation of lipid metabolism and the suppression of the NF-κB signaling cascade. Santalol represents a promising therapeutic candidate for NSCLC.
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