期刊
CANCER LETTERS
卷 337, 期 2, 页码 177-183出版社
ELSEVIER IRELAND LTD
DOI: 10.1016/j.canlet.2013.05.014
关键词
Cell cycle arrest; Castration-resistant prostate cancer; Cyclins; Cyclin-dependent kinase; Growth inhibition
类别
资金
- USPHS [R01-AT002890]
- NCCAM
This study examined the effect of 3, 9-dihydroxy-2-prenylcoumestan (pso), a furanocoumarin, on PC-3 and C4-2B castration-resistant prostate cancer (CRPC) cell lines. Pso caused significant G(0)/G(1) cell cycle arrest and inhibition of cell growth. Molecular analysis of cyclin (D1, D2, D3, and E), cyclin-dependent kinase (cdk) (cdks 2, 4, and 6), and cdk inhibitor (p21 and p27) expression suggested transcriptional regulation of the cdk inhibitors and more significant downregulation of cdk4 than of cyclins or other cdks. Overexpression of cdk4, or silencing of p21 or p27, overcame pso-induced G(0)/G(1) arrest, suggesting that G(0)/G(1) cell cycle arrest is a potential mechanism of growth inhibition in CRPC cells. Published by Elsevier Ireland Ltd.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据