Loss of 14-3-3sigma in prostate cancer and its precursors

Liang Cheng1, Chong-Xian Pan, Jian-Ting Zhang

  • 1Department of Pathology and Laboratory Medicine, Indiana University School of Medicine, Indianapolis, IN 46202, USA. lcheng@iupui.edu

Abstract

Insights

Loss of 14-3-3sigma protein expression is linked to prostate cancer development. This protein

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Cycle Regulation

Background:

  • 14-3-3 proteins are conserved in mammals.
  • 14-3-3sigma (HME-1/stratifin) is found in epithelial cells.
  • Loss of 14-3-3sigma correlates with cell cycle G(2)-M arrest failure and chromosomal aberrations.

Purpose of the Study:

  • To investigate the role of 14-3-3sigma in prostate carcinogenesis.
  • To determine if 14-3-3sigma expression changes during prostate cancer progression.

Main Methods:

  • Studied 111 prostate adenocarcinoma specimens with adjacent normal and high-grade prostatic intraepithelial neoplasia (HGPIN).
  • Utilized immunohistochemistry to detect 14-3-3sigma expression.
  • Correlated 14-3-3sigma levels with clinical and pathological parameters.

Main Results:

  • Normal prostate epithelium exhibits high 14-3-3sigma expression.
  • Prostatic intraepithelial neoplasia and adenocarcinoma show significantly decreased 14-3-3sigma expression.
  • Suppression of 14-3-3sigma occurs during the transition from normal epithelium to HGPIN in 90% of cases.

Conclusions:

  • Loss of 14-3-3sigma expression contributes to prostate adenocarcinoma development.
  • Decreased 14-3-3sigma is a hallmark of progression from normal to cancerous prostate epithelium.