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e-journal

Casticin suppresses self-renewal and invasion of lung cancer stem-like cells from A549 cells through down-regulation of pAkt

Fei Liu - Nama Orang; Xiaozheng Cao - Nama Orang; Zhihong Liu - Nama Orang; Hui Guo - Nama Orang; Jianguo Cao - Nama Orang;

A subpopulation of cancer stem cells is recognized as the cause of tumorigenesis and spreading. To investigate the effects of casticin (5,30-dihydroxy-3,6,7,40-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 selfrenewal 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 mmol/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 selfrenewal 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.

Keywords lung cancer; casticin; cancer stem cells; pAkt; therapeutic action


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Informasi Detail
Judul Seri
Acta Biochim Biophys Sin
No. Panggil
-
Penerbit
: Oxford University Press on behalf of the Institute of Biochemistry and Cell Biology, Shanghai Instit., 2014
Deskripsi Fisik
Acta Biochim Biophys Sin 2014, 46: 15–21
Bahasa
English
ISBN/ISSN
-
Klasifikasi
-
Tipe Isi
-
Tipe Media
-
Tipe Pembawa
-
Edisi
-
Subjek
FISIKA
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-
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agus
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  • Casticin suppresses self-renewal and invasion of lung cancer stem-like cells from A549 cells through down-regulation of pAkt
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