Published in

Cell Press, Cancer Cell, 4(6), p. 361-371, 2004

DOI: 10.1016/j.ccr.2004.08.029

Links

Tools

Export citation

Search in Google Scholar

Distinct Effects on Gene Expression of Chemical and Genetic Manipulation of the Cancer Epigenome Revealed by a Multimodality Approach.

Journal article published in 2004 by Hengmi M. Cui, C. Matthew Bradbury, John Cook, D. DeeDee K. Smart, Shuping P. Zhao, Lynn Young, Sheri A. Brandenburg, Yali L. Hu, David; Cui Hengmi; Bradbury C. Matthew; Cook John; Smart DeeDee K.; Zhao Shuping; Young Lynn; Brandenburg Sheri A.; Hu Yali; Bisht Kheem S.; Ho Allen S.; Mattson David; Sun Lunching; Munson Peter J.; Chuang Eric Y.; Mitchell James B.; Feinberg Andrew P. Gius, Kheem S. Bisht, Allen S. Ho ORCID, David Mattson, Lunching C. Sun, Peter J. Munson, Eric Y. Chuang and other authors.
This paper is available in a repository.
This paper is available in a repository.

Full text: Download

Green circle
Preprint: archiving allowed
Upload
Orange circle
Postprint: archiving restricted
Upload
Red circle
Published version: archiving forbidden
Policy details
Data provided by SHERPA/RoMEO

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.