Molecular interplay between cdk4 and p21 dictates G0/G1 cell cycle arrest in prostate cancer cells

被引：52

作者：

Gulappa, Thippeswamy ^{[1
]}

Reddy, Ramadevi Subramani ^{[1
]}

Suman, Suman ^{[1
]}

Nyakeriga, Alice M. ^{[1
]}

Damodaran, Chendil ^{[1
]}

机构：

[1] Texas Tech Univ, Hlth Sci Ctr, Dept Biomed Sci, Paul L Foster Sch Med, El Paso, TX 79905 USA

来源：

CANCER LETTERS | 2013年 / 337卷 / 02期

关键词：

Cell cycle arrest; Castration-resistant prostate cancer; Cyclins; Cyclin-dependent kinase; Growth inhibition; PSORALIDIN; APOPTOSIS; PROLIFERATION; INHIBITORS; PROTEIN; GROWTH; CHEMOPREVENTION; EXPRESSION;

D O I：

10.1016/j.canlet.2013.05.014

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

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.

引用

页码：177 / 183

页数：7

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