| Literature DB >> 18542058 |
C Sun1, A Dobi, A Mohamed, H Li, R L Thangapazham, B Furusato, S Shaheduzzaman, S-H Tan, G Vaidyanathan, E Whitman, D J Hawksworth, Y Chen, M Nau, V Patel, M Vahey, J S Gutkind, T Sreenath, G Petrovics, I A Sesterhenn, D G McLeod, S Srivastava.
Abstract
The high prevalence of TMPRSS2-ERG rearrangements ( approximately 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.Entities:
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Year: 2008 PMID： 18542058 PMCID： PMC7556723 DOI： 10.1038/onc.2008.183
Source DB: PubMed Journal: Oncogene ISSN： 0950-9232 Impact factor: 9.867