Emodin elicits cytotoxicity in human lung adenocarcinoma A549 cells through inducing apoptosis
Publication in refereed journal

香港中文大學研究人員

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摘要This study investigated the mechanism of the cytotoxic effect of emodin, an active anthraquinone, on human lung adenocarcinoma A549 cells. In vitro growth inhibition and suppression on colony forming were used to evaluate the effects of emodin on A549 cells. Emodin's ability in changing the expressions of apoptosis-related genes was studied by real-time RT-PCR. Emodin could significantly inhibit the growth of A549 cells with IC50 = 16.85 mu g/ml (similar to 60 mu M). It also concentration dependently inhibited the colony-forming ability of A549 cells with IC50 = 7.60 mu g/ml (similar to 30 mu M). Hallmarks of apoptosis, such as single-strand DNA breakage and DNA fragmentation, were observed in A549 cells treated with emodin. Emodin (72 h) treatment could up-regulate the gene expression of FASL (p < 0.05) and down-regulate the gene expression of C-MYC (p < 0.01), but induce no significant changes in the gene expressions of MCL1, GAPDH, BAX and CCND1. These results suggest that emodin could induce growth inhibition and apoptosis in A549 cells through modifying the extrinsic apoptotic pathways and the induction of cell cycle arrest.
著者Li WY, Ng YF, Zhang H, Guo ZD, Guo DJ, Kwan YW, Leung GPH, Lee SMY, Yu PHF, Chan SW
期刊名稱Inflammopharmacology
出版年份2014
月份4
日期1
卷號22
期次2
出版社Springer Verlag (Germany)
頁次127 - 134
國際標準期刊號0925-4692
電子國際標準期刊號1568-5608
語言英式英語
關鍵詞Cell cycle arrest; DNA fragmentation; Emodin; Growth inhibition
Web of Science 學科類別Immunology; Pharmacology & Pharmacy; Toxicology

上次更新時間 2020-19-09 於 01:41