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Transcriptional induction of DLC-1 gene through Sp1 sites by histone deacetylase inhibitors in gastric cancer cells

Cited 10 time in Web of Science Cited 14 time in Scopus
Authors
Kim, Tai Young; Kim, In Sook; Jong, Hyun-Soon; Lee, Jung Weon; Kim, Tae-You; Jung, Mira; Bang, Yung-Jue
Issue Date
2008-12
Citation
Experimental and Molecular Medicine, Vol.40 No.6, pp.639-646
Keywords
DLC1 protein, humanhistone deacetylasesp300-CBP transcription factorspromoter regions, geneticSp1 transcription factortrichostation A
Abstract
We previously reported that trichostatin A (TSA), a histone deacetylase (HDAC) inhibitor, induced DLC-1 mRNA expression and accumulated acetylated histones H3 and H4 associated with the DLC-1 promoter in DLC-1 non-expressing gastric cancer cells. In this study, we demonstrated the molecular mechanisms by which TSA induced the DLC-1 gene expression. Treatment of the gastric cancer cells with TSA activates the DLC-1 promoter activity through Sp1 sites located at -219 and -174 relative to the transcription start site. Electrophoretic mobility-shift assay (EMSA) revealed that Sp1 and Sp3 specifically interact with these Sp1 sites and showed that TSA did not change their binding activities. The ectopic expression of Sp1, but not Sp3, enhances the DLC-1 promoter responsiveness by TSA. Furthermore, the TSA-induced DLC-1 promoter activity was increased by p300 expression and reduced by knockdown of p300. These results demonstrated the requirement of specific Sp1 sites and dependence of Sp1 and p300 for TSA-mediated activation of DLC-1 promoter.
ISSN
1226-3613
URI
https://hdl.handle.net/10371/173068
DOI
https://doi.org/10.3858/emm.2008.40.6.639
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College of Medicine/School of Medicine (의과대학/대학원)Internal Medicine (내과학전공)Journal Papers (저널논문_내과학전공)
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