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Histone deacetylase inhibitor apicidin induces cyclin E expression through Sp1 sites

Authors
Soyoung KimJae Ku KangKim, Yong KeeDong-Wan SeoSeong Hoon AhnJae Cheol LeeChang-Hee LeeJueng-Soo YouEun-Jung ChoHyang Woo LeeJeung-Whan Han
Issue Date
Apr-2006
Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
Citation
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, v.342, no.4, pp 1168 - 1173
Pages
6
Journal Title
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
Volume
342
Number
4
Start Page
1168
End Page
1173
URI
https://scholarworks.sookmyung.ac.kr/handle/2020.sw.sookmyung/146266
DOI
10.1016/j.bbrc.2006.02.081
ISSN
0006-291X
1090-2104
Abstract
We show that a histone deacetylase (HDAC) inhibitor apicidin increases the transcriptional activity of cyclin E gene, which results in accumulation of cyclin E mRNA and protein in a time- and close-dependent manner. Interestingly, apicidin induction of cyclin E gene is found to be mediated by Sp1- rather than E21F-bincling sites in the cyclin E promoter, as evidenced by the fact that specific inhibition of Sp1 leads to a decrease in apicidin activation of cyclin E promoter activity and protein expression, but mutation of E2F-binding sites of cyclin E promoter region fails to inhibit the ability of apicidin to activate cyclin E transcription. In addition, this transcriptional activation of cyclin E by apicidin is associated with historic hyperacetylation of cyclin E promoter region containing Sp1-binding sites. Our results demonstrate that regulation of historic modification by an HDAC inhibitor apicidin contributes to induction of cyclin E expression and this effect is Sp1-dependent. (c) 2006 Elsevier Inc. All rights reserved.
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