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Epigenetic repression of SATB1 by Polycomb group protein EZH2 in epithelial cells.
MedLine Citation:
PMID:  21232178     Owner:  NLM     Status:  In-Data-Review    
Abstract/OtherAbstract:
Objective To study the regulatory mechanism of SATB1 repression in cells other than T cells or erythroid cells, which have high expression level of SATB1. Methods HeLa epithelial cells were treated with either histone deacetylase inhibitor (HDACi) trichostatin A (TSA) or DNA methylation inhibitor 5-Aza-C before detecting SATB1 expression. Luciferase reporter system was applied to measure effects of EZH2 on SATB1 promoter activity. Over-expression or knockdown of EZH2 and subsequent quantitative reverse transcription-polymerase chain reaction were performed to determine the effect of this Polycomb group protein on SATB1 transcription. Chromatin immunoprecipitation (ChIP) assay was applied to measure enrichment of EZH2 and trimethylated H3K27 (H3K27me3) at SATB1 promoter in HeLa cells. K562 cells and Jurkat cells, both having high-level expression of SATB1, were used in the ChIP experiment as controls. Results Both TSA and 5-Aza-C increased SATB1 expression in HeLa cells. Over-expression of EZH2 reduced promoter activity as well as the mRNA level of SATB1, while knockdown of EZH2 apparently enhanced SATB1 expression in HeLa cells but not in K562 cells and Jurkat cells. ChIP assay Results suggested that epigenetic silencing of SATB1 by EZH2 in HeLa cells was mediated by trimethylation modification of H3K27. In contrast, enrichment of EZH2 and H3K27me3 was not detected within proximal promoter region of SATB1 in either K562 or Jurkat cells. Conclusion SATB1 is a bona fide EZH2 target gene in HeLa cells and the repression of SATB1 by EZH2 may be mediated by trimethylation modification on H3K27.
Authors:
Li Lei; Lu Lu; Lv Xiang; Wu Xue-Song; Liu De-Pei; Liang Chih-Chuan
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Chinese medical sciences journal = Chung-kuo i hsüeh k'o hsüeh tsa chih / Chinese Academy of Medical Sciences     Volume:  25     ISSN:  1001-9294     ISO Abbreviation:  Chin. Med. Sci. J.     Publication Date:  2010 Dec 
Date Detail:
Created Date:  2011-01-14     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  9112559     Medline TA:  Chin Med Sci J     Country:  China    
Other Details:
Languages:  eng     Pagination:  199-205     Citation Subset:  IM    
Affiliation:
National Laboratory of Medical Molecular Biology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100005, China.
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