Down regulation of PSA by C/EBPalpha is associated with loss of AR expression and inhibition of PSA promoter activity in the LNCaP cell line

BMC Cancer. 2006 Jun 14:6:158. doi: 10.1186/1471-2407-6-158.

Abstract

Background: C/EBPalpha is a transcription factor essential for terminal differentiation of several cell types. It has not known if C/EBPalpha protein is expressed and functions in the prostate gland.

Methods: The presence of C/EBPalpha in normal and cancerous prostate epithelium was examined by immunochemistry. Over expression of C/EBPalpha in LNCaP cells was conducted with retrovirus-mediated transduction. PSA expression was examined by RT-PCR and western blot and PSA promoter activity by luciferase reporter assay.

Results: In normal prostate C/EBPalpha was expressed in the basal layer of the epithelium. In prostate cancer C/EBPalpha was detected at low levels throughout the cancers and in advanced prostate cancer C/EBPalpha expression was associated with decreased expression of AR and PSA. Overexpression of C/EBPalpha inhibited epigenetically PSA expression and was accompanied by the loss of expression of AR. Transient increase of C/EBPalpha inhibited the PSA promoter/enhancer activity independently of expression of AR.

Conclusion: In LNCaP cells C/EBPalpha over expression inhibits expression of PSA by AR -dependent and independent mechanisms and by extinguishing AR expression provides a model for hormonal independent cell growth.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • CCAAT-Enhancer-Binding Protein-alpha / metabolism*
  • Cell Line, Tumor
  • Down-Regulation / genetics*
  • Gene Expression Regulation, Neoplastic*
  • Humans
  • Immunohistochemistry
  • Male
  • Promoter Regions, Genetic / genetics*
  • Prostate / metabolism
  • Prostate-Specific Antigen / genetics*
  • Prostatic Neoplasms / genetics
  • Prostatic Neoplasms / metabolism
  • Prostatic Neoplasms / pathology
  • Protein Isoforms / genetics
  • Protein Isoforms / metabolism
  • Rats
  • Receptors, Androgen / metabolism*
  • Transcription, Genetic / genetics

Substances

  • CCAAT-Enhancer-Binding Protein-alpha
  • Protein Isoforms
  • Receptors, Androgen
  • Prostate-Specific Antigen