ArticleMolecules (Basel, Switzerland)2014
Griffipavixanthone from Garcinia oblongifolia champ induces cell apoptosis in human non-small-cell lung cancer H520 cells in vitro.
Article in Molecules (Basel, Switzerland), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Substrate- and Reagent-Controlled Dimerization of VinylThe Journal of organic chemistry · 2025Article
- Xanthone Dimers in Angiosperms, Fungi, Lichens: Comprehensive Review of Their Sources, Structures, and Pharmacological Properties.Molecules (Basel, Switzerland) · 2025Review
- Study on the effects of the different polar group of EPA-enriched phospholipids on the proliferation and apoptosis in 95D cells.Marine life science & technology · 2021Article
- Asymmetric Synthesis of Griffipavixanthone Employing a Chiral Phosphoric Acid-Catalyzed Cycloaddition.Journal of the American Chemical Society · 2019Article
- Contribution of reactive oxygen species to the anticancer activity of aminoalkanol derivatives of xanthone.Investigational new drugs · 2018Article
- Biomimetic Total Synthesis of (±)-Griffipavixanthone via a Cationic Cycloaddition-Cyclization Cascade.Journal of the American Chemical Society · 2017Article
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Authors and funding
5 authors.
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Abstract
Griffipavixanthone (GPX) is a dimeric xanthone which was isolated in a systematic investigation of Garcinia oblongifolia Champ. In this study, we investigate the effect of GPX on cell proliferation and apoptosis on human Non-small-cell lung cancer (NSCLC) cells in vitro and determine the mechanisms of its action. GPX inhibited the growth of H520 cells in dose- and time-dependent manners, with IC50 values of 3.03 ± 0.21 μM at 48 h. The morphologic characteristics of apoptosis and apoptotic bodies were observed by fluorescence microscope and transmission electron microscope. In addition, Annexin V/PI double staining assay revealed that cells in early stage of apoptosis were significantly increased upon GPX treatment dose-dependently. Rh123 staining assay indicated that GPX reduced the mitochondrial membrane potential. DCFH-DA staining revealed that intracellular ROS increased with GPX treatment. Moreover, GPX cleaved and activated caspase-3. In summary, this study showed that GPX inhibited H520 cell proliferation in dose- and time-dependent manner. Further mechanistic study indicated that GPX induced cell apoptosis through mitochondrial apoptotic pathway accompanying with ROS production. Our results demonstrate the potential application of GPX as an anti-non-small cell lung cancer agent.
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