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A natural antisense transcript regulates acetylcholinesterase gene expression via epigenetic modification in Hepatocellular Carcinoma.

Authors
  • Xi, Qiliang1
  • Gao, Ning2
  • Zhang, Xuejin1
  • Zhang, Bo1
  • Ye, Weiyuan1
  • Wu, Jun1
  • Zhang, Xuejun3
  • 1 State Key Laboratory of Cell Biology, Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Graduate School of the Chinese Academy of Sciences, 320 YueYang Road, Shanghai 200031, PR China. , (China)
  • 2 State Key Laboratory of Molecular Biology, Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Graduate School of the Chinese Academy of Sciences, 320 YueYang Road, Shanghai 200031, PR China. , (China)
  • 3 State Key Laboratory of Cell Biology, Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Graduate School of the Chinese Academy of Sciences, 320 YueYang Road, Shanghai 200031, PR China. Electronic address: [email protected]. , (China)
Type
Published Article
Journal
The international journal of biochemistry & cell biology
Publication Date
Oct 01, 2014
Volume
55
Pages
242–251
Identifiers
DOI: 10.1016/j.biocel.2014.09.012
PMID: 25240585
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

In recent years, widespread antisense transcripts have been identified systematically in mammalian cells and are known to regulate gene expression, although their functional significance remains largely unknown. Previous work has identified that acetylcholinesterase (AChE) is expressed aberrantly in various malignant tumors and function as a tumor growth suppressor. However, the mechanism of AChE gene regulation in tumors remains unclear. In this study, we show that the AChE antisense RNA (AChE-AS) play an important role in AChE expression regulation. An inverse relationship was identified between AChE-AS and AChE expression in hepatocellular carcinoma and hepatoma cells. The silenced AChE-AS corresponds to elevated expression of AChE. Furthermore, we demonstrated that reduced AChE-AS increased H3K4 methylation and decreased H3K9 methylation in the AChE promoter region. As expected, elevated AChE levels induced by inhibition of AChE-AS enhanced anticarcinogen-induced apoptosis. These observations demonstrated that AChE-AS modulates AChE expression and exerts an anti-apoptotic effect through direct repression of AChE expression in HCC cells. Thus, natural antisense RNA may play an important role in AChE regulation via affecting the epigenetic modification in the AChE promoter region. Copyright © 2014 Elsevier Ltd. All rights reserved.

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