Chinese Medical Sciences Journal ›› 2010, Vol. 25 ›› Issue (4): 199-205.doi: 10.1016/S1001-9294(11)60002-3

• Original Article • Previous Articles     Next Articles

Epigenetic repression of SATB1 by Polycomb group protein EZH2 in epithelial cells

Lei Li, Lu Lu, Xiang Lü, Xue-song Wu, De-pei Liu*, and Chih-chuan Liang#   

  1. National Laboratory of Medical Molecular Biology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100005, China
  • Received:2010-09-26 Online:2010-12-20 Published:2010-12-20
  • Contact: NationalLaboratory of Medical Molecular Biology, Instituteof Basic Medical Sciences, Chinese Academyof Medical Sciences & Peking Union Medical College,Beijing 100005, China

Abstract: 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.

Key words: SATB1, EZH2, Polycomb group protein, gene silencing, trimethylated H3K27


NationalNatural Science Foundation of China (30721063), National Basic Research Programof China (973 Program) (2005CB522402, 2006CB910403), National Laboratory ofMedical Molecular Biology grant (2060204), and Beijing municipal government grant(YB20081002301).

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