ArticleIn vivo (Athens, Greece)
Mitochondrial Damage-induced Ferroptosis: The Molecular Mechanism by Which Psoralen Inhibits the Proliferation and Invasion of Non-small-cell Lung Cancer Cells.
Article in In vivo (Athens, Greece). 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
BACKGROUND/
aimFerroptosis, an iron-dependent form of cell death mediated by lipid peroxidation, plays a critical role in non-small-cell lung cancer (NSCLC) progression. Psoralen, a bioactive natural compound, exhibits anticancer properties, but its effects and mechanisms in NSCLC remain unclear. This study explored whether psoralen induces ferroptosis by triggering mitochondrial damage and investigates the underlying molecular mechanisms. MATERIALS AND
methodsCell Counting Kit-8 was used to assess the impact of psoralen on cell viability, while 5-ethynyl-2'-deoxyuridine incorporation, colony-formation, scratch wound-healing, and Transwell assays evaluated its effects on proliferation, migration, and invasion. FerroOrange and 2',7'-dichlorodihydrofluorescein diacetate fluorescence probes, Western blot, and kits for malondialdehyde (MDA), lipid peroxidation (LPO), reduced glutathione (GSH), and oxidized glutathione disulfide (GSSG) were used to assess ferroptosis-related markers. JC-1, MitoTracker Green, and MitoSOX Red probes, along with transmission electron microscopy, were used to evaluate mitochondrial damage. Bioinformatics analysis, network pharmacology, and molecular docking were conducted to elucidate potential mechanisms.
resultsPsoralen disrupted mitochondrial structure and function; increased Fe
conclusionPsoralen induces ferroptosis in NSCLC by disrupting mitochondrial structure and function. These findings highlight its potential as a natural ferroptosis-targeting agent and provide insights for developing psoralen-based anticancer therapeutics.
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