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HDAC3 selectively represses CREB3-mediated transcription and migration of metastatic breast cancer cells

Authors
 Han-Cheon Kim  ;  Kyung-Chul Choi  ;  Hyo-Kyoung Choi  ;  Hee-Bum Kang  ;  Mi-Jeong Kim  ;  Yoo-Hyun Lee  ;  Ok-Hee Lee  ;  Jeongmin Lee  ;  Young Jun Kim  ;  Woojin Jun  ;  Jae-Wook Jeong  ;  Ho-Geun Yoon 
Citation
 CELLULAR AND MOLECULAR LIFE SCIENCES, Vol.67(20) : 3499-3510, 2010 
Journal Title
 CELLULAR AND MOLECULAR LIFE SCIENCES 
ISSN
 1420-682X 
Issue Date
2010
MeSH
Breast Neoplasms/enzymology* ; Breast Neoplasms/genetics ; Breast Neoplasms/pathology* ; Cell Line, Tumor ; Cell Movement* ; Cyclic AMP Response Element-Binding Protein/chemistry ; Cyclic AMP Response Element-Binding Protein/metabolism* ; Down-Regulation/genetics ; Female ; Gene Expression Regulation, Neoplastic ; Histone Deacetylases/chemistry ; Histone Deacetylases/metabolism* ; Humans ; NF-kappa B/metabolism ; Neoplasm Metastasis/genetics ; Neoplasm Metastasis/pathology ; Protein Binding ; Protein Interaction Mapping ; Protein Structure, Tertiary ; Receptors, CXCR4/genetics ; Receptors, CXCR4/metabolism ; Repressor Proteins/metabolism* ; Transcription, Genetic*
Keywords
Histone deacetylase 3 ; cAMP response element-binding protein 3 (CREB3) ; Chemokine ; CXC motif ; Receptor 4 (CXCR4) ; Migration ; Breast cancer cell
Abstract
We identified CREB3 as a novel HDAC3-interacting protein in a yeast two-hybrid screen for HDAC3-interacting proteins. Among all class I HDACs, CREB3 specifically interacts with HDAC3, in vitro and in vivo. HDAC3 efficiently inhibited CREB3-enhanced NF-κB activation, whereas the other class I HDACs did not alter NF-κB-dependent promoter activities or the expression of NF-κB target genes. Importantly, both knock-down of CREB3 and overexpression of HDAC3 suppressed the transcriptional activation of the novel CREB3-regulated gene, CXCR4. Furthermore, CREB3 was shown to bind to the CRE element in the CXCR4 promoter and to activate the transcription of the CXCR4 gene by causing dissociation of HDAC3 and subsequently increasing histone acetylation. Importantly, both the depletion of HDAC3 and the overexpression of CREB3 substantially increased the migration of MDA-MB-231 metastatic breast cancer cells. Taken together, these findings suggest that HDAC3 selectively represses CREB3-mediated transcriptional activation and chemotactic signalling in human metastatic breast cancer cells.
Full Text
http://link.springer.com/article/10.1007%2Fs00018-010-0388-5
DOI
10.1007/s00018-010-0388-5
Appears in Collections:
1. College of Medicine (의과대학) > BioMedical Science Institute (의생명과학부) > 1. Journal Papers
5. Research Institutes (연구소) > Yonsei Integrative Research Institute for Cerebral & Cardiovascular Disease (뇌심혈관질환융합연구사업단) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Biochemistry and Molecular Biology (생화학-분자생물학교실) > 1. Journal Papers
Yonsei Authors
Kang, Hee Bum(강희범)
Kim, Mi Jeong(김미정) ORCID logo https://orcid.org/0000-0002-0758-7145
Kim, Han Cheon(김한천)
Yoon, Ho Geun(윤호근) ORCID logo https://orcid.org/0000-0003-2718-3372
Lee, Ok Hee(이옥희)
Choi, Kyung Chul(최경철)
Choi, Hyo Kyoung(최효경)
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/101764
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