Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
8293458 | Biochemical and Biophysical Research Communications | 2018 | 6 Pages |
Abstract
The goal of this study is to determine the anti-cancer mechanism of Cordycepin in A549 Cisplatin-Resistance (CR) lung cancer cells. Cordycepin inhibited the viability of A549CR cells in a dose-dependent manner. The cell inhibition was due to induction of apoptosis in the cells treated with Cordycepin by activation of caspase â3, â8 and â9 activities. The cell cycle analysis showed that accumulation of Sub G1 was observed in Cordycepin-treated with A549CR lung cancer cells. Based on the data of expression profile analysis of cell signaling proteins using IPS-FPAA, H-Ras was down-regulated in Cordycepin-treated A549CR cells. Collectively, anti-proliferative function of Cordycepin was due to stimulation of the cell apoptosis and the cell cycle arrest via caspases activation and down-regulation of H-Ras.
Keywords
PI3KpKaERKmTORINRFBSPBS3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-tetrazolium bromideBSAH-rasMAPKMTTbovine serum albuminEnzyme-linked immunosorbent assayELISAApoptosisNSCLCNon-small cell lung cancerfetal bovine serumphosphate buffer salinePhosphoinositide 3-kinasesMechanistic target of rapamycinprotein kinase Amitogen-activated protein kinaseCordycepinextracellular signal-regulated kinase
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Authors
Seong Hyeok Cho, In-Cheol Kang,