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Histone deacetylase inhibitor apicidin induces cyclin E expression through Sp1 sites.

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 dose-dependent manner. Interestingly, apicidin induction of cyclin E gene is found to be mediated by Sp1- rather than E2F-binding 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 histone hyperacetylation of cyclin E promoter region containing Sp1-binding sites. Our results demonstrate that regulation of histone modification by an HDAC inhibitor apicidin contributes to induction of cyclin E expression and this effect is Sp1-dependent.

journal_name

Biochem Biophys Res Commun

journal_title

Biochemical and biophysical research communications

authors

Kim S,Kang JK,Kim YK,Seo DW,Ahn SH,Lee JC,Lee CH,You JS,Cho EJ,Lee HW,Han JW

doi

10.1016/j.bbrc.2006.02.081

subject

Has Abstract

pub_date

2006-04-21 00:00:00

pages

1168-73

issue

4

eissn

0006-291X

issn

1090-2104

pii

S0006-291X(06)00382-2

journal_volume

342

pub_type

杂志文章

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