Journal
ONCOGENE
Volume 27, Issue 40, Pages 5348-5353Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/onc.2008.183
Keywords
ERG; prostate cancer; oncogene; C-MYC; PSA; TMPRSS2-ERG
Funding
- US Army Medical Research and Materiel Command
- NIH Grants [RO1 DK065977, RO1 CA106653]
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The high prevalence of TMPRSS2-ERG rearrangements (similar to 60%) in prostate cancer (CaP) leads to androgenic induction of the ETS-related gene (ERG) expression. However, the biological functions of ERG overexpression in CaP remain to be understood. ERG knockdown in TMPRSS2-ERG expressing CaP cells induced striking morphological changes and inhibited cell growth both in cell culture and SCID mice. Evaluation of the transcriptome and specific gene promoters in ERG siRNA-treated cells and investigation of gene expression signatures of human prostate tumors revealed ERG-mediated activation of C-MYC oncogene and the repression of prostate epithelial differentiation genes (PSA and SLC45A3/Prostein). Taken together, these data combining cell culture and animal models and human prostate tumors reveal that ERG overexpression in prostate tumor cells may contribute to the neoplastic process by activating C-MYC and by abrogating prostate epithelial differentiation as indicated by prostate epithelial specific markers.
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