Dieckol inhibits non‐small–cell lung cancer cell proliferation and migration by regulating the PI3K/AKT signaling pathway

Non‐small–cell lung cancer (NSCLC) is one of the most prevalent type of lung cancers with an increased mortality rate in both developed and developing countries worldwide. Dieckol is one such polyphenolic drug extracted from brown algae which has proven antioxidant and anti‐inflammatory properties....

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Veröffentlicht in:Journal of biochemical and molecular toxicology 2019-08, Vol.33 (8), p.e22346-n/a
Hauptverfasser: Wang, Chun‐Hong, Li, Xiao‐Feng, Jin, Li‐Fang, Zhao, Yan, Zhu, Geng‐Jun, Shen, Wei‐Zhang
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Sprache:eng
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Zusammenfassung:Non‐small–cell lung cancer (NSCLC) is one of the most prevalent type of lung cancers with an increased mortality rate in both developed and developing countries worldwide. Dieckol is one such polyphenolic drug extracted from brown algae which has proven antioxidant and anti‐inflammatory properties. In the present study, we evaluated the anticancer property of dieckol against NSCLC cell line A549. The LC50 value of dieckol was found to be 25 µg/mL by performing 3‐(4,5‐dimethylthiazol‐2‐yl)‐2,5‐diphenyltetrazolium bromide (MTT) assay and the antiapoptotic property of dieckol was analyzed by dual staining technique with acridine orange/propidium iodide (AO/PI) stains. It was further confirmed with flow cytometry analysis with Annexin FITC and JC‐1 staining and the anti‐invasive property was assessed by Transwell assay. The molecular mechanism of dieckol anticancer activity was confirmed by estimating the levels of caspases and by estimating the signaling proteins of Pi3K/AKT/mTOR signaling pathway using the immunoblotting technique. Our data suggest that dieckol is potent anticancer agent, it effectively inhibits the invasive and migratory property A549 cells and it also induces apoptosis via inhibiting Pi3K/AKT/mTOR signaling, activating the tumor suppressor protein E‐cadherin signifying that dieckol is potent natural anticancer drug to treat NSCLC.
ISSN:1095-6670
1099-0461
1099-0461
DOI:10.1002/jbt.22346