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Epigenetic silencing of CCAAT/enhancer-binding protein delta activity by YY1/polycomb group/DNA methyltransferase

Chiung-Yuan Ko1, Hey-Chi Hsu, Meng-Ru Shen

  • 1Institute of Basic Medical Sciences, National Cheng Kung University, Tainan 70101, Taiwan.

The Journal of Biological Chemistry
|August 30, 2008
PubMed

Insights

Human CCAAT/enhancer-binding protein delta (CEBPD) acts as a tumor suppressor. Its gene expression is down-regulated in cervical and liver cancers due to silencing by SUZ12 and YY1, promoting tumor formation.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Epigenetics

Background:

  • Human CCAAT/enhancer-binding protein delta (CEBPD) functions as a tumor suppressor by inducing growth arrest and regulating pro-apoptotic genes.
  • Down-regulation and loss-of-function alterations in CEBPD are observed in cervical cancer and hepatocellular carcinoma.

Purpose of the Study:

  • To investigate the molecular mechanisms underlying CEBPD gene silencing in cervical and hepatocellular carcinoma.
  • To elucidate the roles of Suppressor of zeste 12 (SUZ12) and Yin-Yang-1 (YY1) in CEBPD gene regulation.

Main Methods:

  • Analysis of CEBPD gene expression in cancer patients.
  • Investigation of SUZ12's role in CEBPD promoter activity and methylation.
  • Assessment of YY1's interaction with SUZ12 and recruitment of epigenetic modifiers.

Main Results:

  • CEBPD gene expression is significantly down-regulated in cervical and hepatocellular carcinoma.
  • SUZ12, a component of PRC2, silences CEBPD promoter activity via methylation.
  • YY1 physically interacts with SUZ12, mediating the recruitment of PRC2 and DNA methyltransferases to the CEBPD promoter.

Conclusions:

  • SUZ12-mediated silencing of CEBPD contributes to tumor formation.
  • YY1 acts as a crucial mediator in the silencing pathway involving SUZ12 and DNA methyltransferases, providing in vivo evidence for CEBPD gene silencing.

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