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Fei Liu, Xiaozheng Cao, Zhihong Liu, Hui Guo, Kaiqun Ren, Meifang Quan, Yuan Zhou, Honglin Xiang and Jianguo Cao
College of Medicine, Hunan Normal University, Changsha 410013, China
Acta Biochim Biophys Sin 2014, 46: 15–21; doi: 10.1093/abbs/gmt123
A subpopulation of cancer stem cells is recognized as the cause of tumorigenesis and spreading. To investigate the effects of casticin (5,3′-dihydroxy-3,6,7,4′-tetramethoxyflavone), derived from Fructus Viticis Simplicifoliae, on lung cancer stem cells, we isolated and identified a subpopulation of lung cancer stem-like cells (LCSLCs) from non-small-cell lung carcinoma A549 cells with the features including self-renewal capacity and high invasiveness in vitro, elevated tumorigenic activity in vivo, and high expression of stemness markers CD133, CD44, and aldehyde dehydrogenase 1 (ALDH1), using serum-free suspension sphere-forming culture method. We then found that casticin could suppress the proliferation of LCSLCs in a concentration-dependent manner with an IC50 value of 0.4 μmol/L, being much stronger than that in parental A549 cells. In addition, casticin could suppress the self-renewal and invasion of LCSLCs concomitant with decreased CD133, CD44, and ALDH1 protein expression and reduced MMP-9 activity. Further experiments showed that casticin suppressed self-renewal and invasion at least partly through down-regulation of Akt phosphorylation. In conclusion, casticin suppressed the characteristics of LCSLCs, suggesting that casticin may be a candidate compound for curing lung cancer via eliminating cancer stem cells.
Casticin inhibits the self-renewal of LCSLCs via down-regulation of pAkt
全文: http://abbs.oxfordjournals.org/content/46/1/15.full
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