Title of article
Distinct effects on gene expression of chemical and genetic manipulation of the cancer epigenome revealed by a multimodality approach
Author/Authors
Gius، نويسنده , , David and Cui، نويسنده , , Hengmi and Bradbury، نويسنده , , C.Matthew and Cook، نويسنده , , John and Smart، نويسنده , , DeeDee K. and Zhao، نويسنده , , Shuping and Young، نويسنده , , Lynn and Brandenburg، نويسنده , , Sheri A. and Hu، نويسنده , , Yali and Bisht، نويسنده , , Kheem S. and Ho، نويسنده , , Allen S. and Mattson، نويسنده , , David X Sun، نويسنده , , Lunching and Munson، نويسنده , , Peter J. and Chuang، نويسنده , , Eric Y. and Mitchell، نويسنده , , James B. and Feinberg، نويسنده , , Andrew P.، نويسنده ,
Issue Information
روزنامه با شماره پیاپی سال 2004
Pages
11
From page
361
To page
371
Abstract
We tested the hypothesis that the effects on gene expression of altered DNA methylation by 5-aza-2′-deoxycytidine (5-aza-CdR) and genetic (DNMT knockout) manipulation of DNA are similar, and distinct from Trichostatin A (TSA)-induced chromatin decondensation. Surprisingly, the effects of 5-aza-CdR were more similar to those of TSA than to DNMT1, DNMT3B, or double DNMT somatic cell knockout. Furthermore, the effects of 5-aza-CdR were similar at one and five days exposure, suggesting active demethylation or direct influence of both drugs on the stability of methylation and/or chromatin marks. Agents that induce gene activation through hypomethylation may have unintended consequences, since nearly as many genes were downregulated as upregulated after demethylation. In addition, a 75 kb cluster of metallothionein genes was coordinately regulated.
Journal title
Cancer Cell
Serial Year
2004
Journal title
Cancer Cell
Record number
1335485
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