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TMPRSS2-ERG fusion, a common genomic alteration in prostate cancer activates C-MYC and abrogates prostate epithelial

C Sun1, A Dobi, A Mohamed

  • 1Department of Surgery, Center for Prostate Disease Research, Uniformed Services University of the Health Sciences, Rockville, MD 20852, USA.

Oncogene
|June 11, 2008
PubMed

Insights

Prostate cancer (CaP) involves TMPRSS2-ERG rearrangements, leading to ERG overexpression. This study reveals ERG activates C-MYC and represses differentiation genes, contributing to CaP development.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • TMPRSS2-ERG rearrangements are prevalent in prostate cancer (CaP), approximately 60%.
  • Androgenic induction of ETS-related gene (ERG) expression is linked to these rearrangements.
  • The specific biological functions of ERG overexpression in CaP are not fully understood.

Purpose of the Study:

  • To elucidate the biological functions of ERG overexpression in prostate cancer.
  • To investigate the molecular mechanisms by which ERG influences CaP cell behavior and gene expression.

Main Methods:

  • ERG knockdown using siRNA in TMPRSS2-ERG expressing CaP cells.
  • Assessment of cell morphology and growth in cell culture and SCID mice models.
  • Transcriptome evaluation and gene promoter analysis.
  • Investigation of gene expression signatures in human prostate tumors.

Main Results:

  • ERG knockdown induced significant morphological changes and inhibited cell growth in vitro and in vivo.
  • ERG overexpression was found to activate the C-MYC oncogene.
  • ERG was shown to repress prostate epithelial differentiation genes, including PSA and SLC45A3/Prostein.

Conclusions:

  • ERG overexpression in prostate tumor cells contributes to the neoplastic process.
  • ERG promotes CaP by activating C-MYC oncogene.
  • ERG abrogates prostate epithelial differentiation, indicated by specific markers.

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