Trichostatin A and 5-aza-2′-deoxycytidine switch S1P from an inhibitor to a stimulator of motility through epigenetic regulation of S1P receptors

被引：11

作者：

Koh, Eunjin ^{[1
]}

Bandle, Russell ^{[1
]}

Clair, Timothy ^{[1
]}

Roberts, David D. ^{[1
]}

Stracke, Mary L. ^{[1
]}

机构：

[1] NCI, Pathol Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA

来源：

CANCER LETTERS | 2007年 / 250卷 / 01期

关键词：

sphingosine-1-phosphate; S1P(1); S1P(2); S1P(3); trichostatin A; motility; epigenetic;

D O I：

10.1016/j.canlet.2006.09.017

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

The histone deacetylase inhibitor, trichostatin A (TSA), and the DNA methyltransferase inhibitor, 5-aza-2-deoxycytidine (Aza-dC), induced epigenetic regulation of sphingosine-1-phosphate (S1P) receptors in human melanoma cells, switching SIP from motility inhibitor to stimulator. Quantitative PCR revealed increased expression of S1P(1) and S1P(3), associated with S1P-induced chemotaxis, and decreased expression of S1P(2,) associated with motility inhibition. Expression of lysophosphatidic acid (LPA) receptors was less affected. The TSA effect was reversible suggesting no mutational change, and Aza-dC treatment resulted in demethylation of a putative S1P(1) promoter. S1P receptors, therefore, appear to be susceptible to epigenetic regulation, accompanied by altered cellular functionality. Published by Elsevier Ireland Ltd.

引用

页码：53 / 62

页数：10

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