Activation of NF-kB by HDAC inhibitor apicidin through Sp1-dependent de novo protein synthesis: its implication for resistance to apoptosis
- Authors
- Kim, Yong Kee; E K Lee; J K Kang; J A Kim; J-S You; J H Park; D-W Seo; J W Hwang; S-N Kim; H Y Lee; H W Lee; J-W Han
- Issue Date
- Dec-2006
- Publisher
- SPRINGERNATURE
- Citation
- Cell Death and Differentiation, v.13, no.12, pp 2033 - 2041
- Pages
- 9
- Journal Title
- Cell Death and Differentiation
- Volume
- 13
- Number
- 12
- Start Page
- 2033
- End Page
- 2041
- URI
- https://scholarworks.sookmyung.ac.kr/handle/2020.sw.sookmyung/148524
- DOI
- 10.1038/sj.cdd.4401915
- ISSN
- 1350-9047
1476-5403
- Abstract
- Histone deacetylase ( HDAC) inhibitors are promising anticancer drugs, but these exert differential responses depending on the cell types. Here, we demonstrate a new mechanism for activation of nuclear factor-kappa B (NF-kappa B) by HDAC inhibitor apicidin and the role of NF-kappa B signaling pathway for mediating differential cellular responses, especially, apoptosis. Treatment of HeLa cells with apicidin increases transcriptional activity of NF-kappa B and its target gene IL-8 and cIAP-1 induction, which involves the activation of IKK-I kappa B alpha signaling pathway through Sp1-dependent de novo protein synthesis. In parallel, apicidin treatment leads to histone hyperacetylation in the IL-8 promoter region independent of NF-kappa B signaling pathway, which is not sufficient for full transcription of IL-8 gene. This NF-kappa B activation contributes to resistance of HeLa cells to apoptotic potential of apicidin. Collectively, our results suggest that activation of NF-kappa B signaling cascade functions as a critical modulator to determine cell fate on apoptosis in response to HDAC inhibitors.
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