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Involvement of HDAC1 and the PI3K/PKC signaling pathways in NF-kB activation by the HDAC inhibitor apicidin

Authors
Kim, Yong KeeDong-Wan SeoDong-Won KangHoi Young LeeJeung-Whan HanSu-Nam Kim
Issue Date
Sep-2006
Publisher
Academic Press Inc. Elsevier Science
Citation
Biochemical and Biophysical Research Communications, v.347, no.4, pp 1088 - 1093
Pages
6
Journal Title
Biochemical and Biophysical Research Communications
Volume
347
Number
4
Start Page
1088
End Page
1093
URI
https://scholarworks.sookmyung.ac.kr/handle/2020.sw.sookmyung/146265
DOI
10.1016/j.bbrc.2006.06.196
ISSN
0006-291X
1090-2104
Abstract
Histone deacetylase (HDAC) inhibitors are appreciated as one of promising anticancer drugs, but they exert differential responses depending on the cell type. We recently reported the critical role of NF-kappa B as a modulator in determining cell fate for apoptosis in response to an HDAC inhibitor. In this study, we investigate a possible signaling pathway required for NF-kappa B activation in response to the HDAC inhibitor apicidin. Treatment of HeLa cells with apicidin leads to an increase in transcriptional activity of NF-kappa B and the expression of its target genes, IL-8 and TNF-alpha. TNF-alpha expression by apicidin is induced at earlier time points than NF-kappa B activation or IL-8 expression. In addition, our data show that the early expression of TNF-alpha does not lead to activation of NF-kappa B, because disruption of TNF-alpha activity by a neutralizing antibody does not affect nuclear translocation of NF-kappa B, I kappa B alpha degradation or reporter gene activation by apicidin. However, this activation of NF-kappa B requires the PI3K and PKC signaling pathways, but not ERK or JNK. Furthermore, apicidin activation of NF-kappa B seems to result from HDAC1 inhibition, as evidenced by the observation that overexpression of HDAC1, but not HDAC2, 3 or 4, dramatically inhibits NF-kappa B reporter gene activity. Collectively, our results suggest that activation of NF-kappa B signaling by apicidin requires both the PI3K/PKC signaling pathways and HDAC1, and functions as a critical modulator in determining the cellular effect of apicidin. (c) 2006 Elsevier Inc. All rights reserved.
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