ArticleMolecules (Basel, Switzerland)2013
Panduratin A, a possible inhibitor in metastasized A549 cells through inhibition of NF-kappa B translocation and chemoinvasion.
Article in Molecules (Basel, Switzerland), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Panduratin A Induces Caspase-Dependent Apoptosis and G1-Associated Cell-Cycle Arrest and Enhances TNF-α-Associated Cytotoxicity in NSCLC Cells.Biomolecules · 2026Article
- Nutraceutical Characterization, 3D Airway Tissue Metabolic Viability, and Cytotoxic Activity ofMedicina (Kaunas, Lithuania) · 2026Article
- Panduratin A Induces Autophagy Through AMPK Activation Independent of mTOR Inhibition and Restricts Mycobacterium tuberculosis in Host Macrophages.Molecular microbiology · 2025Article
- Panduratin A fromInternational journal of molecular sciences · 2025Article
- Traditional usages, chemical metabolites, pharmacological activities, and pharmacokinetics ofFrontiers in pharmacology · 2025Review
- Novel isobavachalcone derivatives induce apoptosis and necroptosis in human non-small cell lung cancer H1975 cells.Journal of enzyme inhibition and medicinal chemistry · 2024Article
- Anticancer Potential of Natural Chalcones: In Vitro and In Vivo Evidence.International journal of molecular sciences · 2023Review
- High-content screening of Thai medicinal plants reveals Boesenbergia rotunda extract and its component Panduratin A as anti-SARS-CoV-2 agents.Scientific reports · 2020Article
- The Chemopreventive Activity of Indonesia Medicinal Plants Targeting on Hallmarks of Cancer.Advanced pharmaceutical bulletin · 2019Review
- Diatom-derived polyunsaturated aldehydes activate cell death in human cancer cell lines but not normal cells.PloS one · 2014Article
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5 authors.
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Abstract
In the present study, we investigated the effects of panduratin A (PA), isolated from Boesenbergia rotunda, on apoptosis and chemoinvasion in A549 human non-small cell lung cancer cells. Activation of the executioner procaspase-3 by PA was found to be dose-dependent. Caspase-3 activity was significantly elevated at the 5 µg/mL level of PA treatment and progressed to a maximal level. However, no significant elevated level was detected on procaspase-8. These findings suggest that PA activated caspase-3 but not caspase-8. Numerous nuclei of PA treated A549 cells stained brightly by anti-cleaved PARP antibody through High Content Screening. This result further confirmed that PA induced apoptotic cell death was mediated through activation of caspase-3 and eventually led to PARP cleavage. Treatment of A549 cells with PA resulted in a strong inhibition of NF-κB activation, which was consistent with a decrease in nuclear levels of NF-κB/p65 and NF-κB/p50 and the elevation of p53 and p21. Besides that, we also showed that PA significantly inhibited the invasion of A549 cells in a dose-dependent manner through reducing the secretion of MMP-2 of A549 cells gelatin zymography assay. Our findings not only provide the effects of PA, but may also be important in the design of therapeutic protocols that involve targeting of either p53 or NF-κB.
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