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Epigenetic silencing of 14-3-3sigma in cancer

Dmitri Lodygin1, Heiko Hermeking

  • 1Molecular Oncology, Independent Max-Planck Research Group, Max-Planck-Institute of Biochemistry, Martinsried, Munich, Germany.

Seminars in Cancer Biology
|May 16, 2006
PubMed

Insights

The 14-3-3sigma gene, targeted by p53, is epigenetically silenced in cancers like prostate and breast. This inactivation promotes tumor development and may serve as a diagnostic marker.

Area of Science:

  • Oncology
  • Epigenetics
  • Molecular Biology

Background:

  • The 14-3-3sigma gene, a direct target of the p53 tumor suppressor, plays a role in cell cycle regulation.
  • Proteomic analysis indicates 14-3-3sigma also influences carcinogenesis-related processes like cell migration and MAP-kinase signaling.
  • Down-regulation of 14-3-3sigma expression via CpG methylation is observed in various human cancers, including prostate, lung, breast, and skin cancers.

Purpose of the Study:

  • To investigate the role of 14-3-3sigma in carcinogenesis.
  • To understand the mechanism of 14-3-3sigma down-regulation in cancer.
  • To explore the potential diagnostic and prognostic utility of 14-3-3sigma CpG methylation.

Main Methods:

  • Gene expression analysis.
  • Proteomic analysis.
  • CpG methylation analysis.

Main Results:

  • 14-3-3sigma expression is down-regulated by CpG methylation in multiple human cancers.
  • Epigenetic inactivation of 14-3-3sigma occurs early in tumor development.
  • This inactivation may facilitate evasion from senescence and promote genomic instability.

Conclusions:

  • Epigenetic silencing of 14-3-3sigma is a significant event in early carcinogenesis.
  • CpG methylation of 14-3-3sigma could serve as a valuable diagnostic and prognostic biomarker for various cancers.

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