14-3-3sigma is down-regulated in human prostate cancer

Biochem Biophys Res Commun. 2004 Jul 2;319(3):795-800. doi: 10.1016/j.bbrc.2004.05.056.

Abstract

The 14-3-3sigma is a negative regulator of the cell cycle, which is induced by p53 in response to DNA damage. It has been characterized as an epithelium-specific marker and down-regulation of the protein has been shown in breast cancers, suggesting its tumor-suppressive activity in epithelial cells. Here we demonstrate that 14-3-3sigma protein is down-regulated in human prostate cancer cell lines, LNCaP, PC3, and DU145 compared with normal prostate epithelial cells. Immunohistochemical analysis of primary prostate cells shows that the expression of 14-3-3sigma protein is epithelial cell-specific. Among prostate pathological specimens, > 95% of benign hyperplasia samples show significant and diffuse immunostaining of 14-3-3sigma in the cytoplasm whereas < 20% of carcinoma samples show positive staining. In terms of mechanisms for the down-regulation of 14-3-3sigma in prostate cancer cells, hypermethylation of the gene promoter plays a causal role in LNCaP cells as 14-3-3sigma mRNA level was elevated by 5-aza-2'-deoxycytidine demethylating treatment. Intriguingly, the proteasome-mediated proteolysis is responsible for 14-3-3sigma reduction in DU145 and PC3 cells, as 14-3-3sigma protein expression was increased by treatment with a proteasome inhibitor MG132. Furthermore, tumor necrosis factor-related apoptosis-inducing ligand enhances 14-3-3sigma gene and protein expression in DU145 and PC3 cells. These data suggest that 14-3-3sigma expression is down-regulated during the neoplastic transition of prostate epithelial cells.

MeSH terms

  • 14-3-3 Proteins
  • Apoptosis Regulatory Proteins
  • Biomarkers, Tumor / genetics
  • Biomarkers, Tumor / metabolism*
  • Cell Line, Tumor
  • Cell Transformation, Neoplastic
  • Cysteine Endopeptidases / metabolism
  • Down-Regulation*
  • Exonucleases / genetics
  • Exonucleases / metabolism*
  • Exoribonucleases
  • Gene Expression Regulation, Neoplastic
  • Gene Silencing
  • Humans
  • Male
  • Membrane Glycoproteins / metabolism
  • Methylation
  • Multienzyme Complexes / metabolism
  • Neoplasm Proteins / genetics
  • Neoplasm Proteins / metabolism*
  • Prostatic Neoplasms / metabolism*
  • Prostatic Neoplasms / pathology
  • Proteasome Endopeptidase Complex
  • Protein Isoforms / genetics
  • Protein Isoforms / metabolism
  • TNF-Related Apoptosis-Inducing Ligand
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • 14-3-3 Proteins
  • Apoptosis Regulatory Proteins
  • Biomarkers, Tumor
  • Membrane Glycoproteins
  • Multienzyme Complexes
  • Neoplasm Proteins
  • Protein Isoforms
  • TNF-Related Apoptosis-Inducing Ligand
  • TNFSF10 protein, human
  • Tumor Necrosis Factor-alpha
  • Exonucleases
  • Exoribonucleases
  • SFN protein, human
  • Cysteine Endopeptidases
  • Proteasome Endopeptidase Complex