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W2000451798 abstract "You have accessJournal of UrologyProstate Cancer: Basic Research III1 Apr 2014MP41-03 NOTCH SIGNALING PATHWAY AS COMMON TARGET OF ERG IN DIVERSE TUMOR CELL TYPES Ahmed Mohamed, Lakshmi Ravindranath, Shilpa Katta, Shyh-Han Tan, Yongmei Chen, Gyorgy Petrovics, Albert Dobi, and Shiv Srivastava Ahmed MohamedAhmed Mohamed More articles by this author , Lakshmi RavindranathLakshmi Ravindranath More articles by this author , Shilpa KattaShilpa Katta More articles by this author , Shyh-Han TanShyh-Han Tan More articles by this author , Yongmei ChenYongmei Chen More articles by this author , Gyorgy PetrovicsGyorgy Petrovics More articles by this author , Albert DobiAlbert Dobi More articles by this author , and Shiv SrivastavaShiv Srivastava More articles by this author View All Author Informationhttps://doi.org/10.1016/j.juro.2014.02.1220AboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareFacebookTwitterLinked InEmail Introduction and Objectives The ETS-Related Gene (ERG) is frequently rearranged in several human malignancies including subsets of Ewing's sarcomas, certain leukemias, and the majority of prostate cancers (CaP). These alterations have been causally implicated in tumor initiation and progression. Thus, ERG is a promising therapeutic target for ERG-positive malignancies. However, targeting nuclear transcription factors, such as ERG, have proven therapeutically difficult. Thus, identifying functionally relevant targets of ERG may provide rational therapeutic alternative. The goal of this study is to identify common tumor specific ERG target genes that can be utilized as a therapeutic target for the majority of CaP and other ERG expressing tumors. Methods Gene expression analysis of ERG associated signatures in cell culture models of normal endothelium, colon and prostate cancers were analyzed by microarrays in response to ERG specific siRNA. ERG, NOTCH1 and NOTCH2 and downstream targets of NOTCH transcription factors were analyzed by Western blot, and qRT-PCR assay. Relationship of ERG and NOTCH expression was evaluated in a CaP gene expression dataset in 40 patients(NCBI-GSE32448). Results By evaluating cell culture models of normal endothelium and colon and prostate cancers we identified NOTCH transcription factors as common transcription targets of ERG. Inhibition of ERG resulted in decreases of both NOTCH1 and NOTCH 2 proteins, their targets, as well as, proteins associated with epithelial-mesenchymal transition. Silencing of NOTCH1 or NOTCH2 recapitulated the phenotypes of ERG inhibition. Moreover, inhibitors of NOTCH resulted in decreased levels of ERG and inhibition of cell growth. Another important observation is that in malignant cells ERG negatively regulates differentiation. In contrast, in normal endothelial cells ERG activates the differentiation-associated gene expression network. In a meta-analysis of a CaP gene expression database, expression of NOTCH2 was positively correlated with ERG. Conclusions We identified NOTCH transcription factors as common targets of ERG in diverse cell types and NOTCH inhibitors as potential ERG therapeutic agents, alone or in combination with other inhibitors. The cell context specific signatures of ERG associated data will enhance our understanding of ERG biological functions, thus facilitating the design of ERG targeted therapeutic strategies. © 2014FiguresReferencesRelatedDetails Volume 191Issue 4SApril 2014Page: e451 Advertisement Copyright & Permissions© 2014MetricsAuthor Information Ahmed Mohamed More articles by this author Lakshmi Ravindranath More articles by this author Shilpa Katta More articles by this author Shyh-Han Tan More articles by this author Yongmei Chen More articles by this author Gyorgy Petrovics More articles by this author Albert Dobi More articles by this author Shiv Srivastava More articles by this author Expand All Advertisement Advertisement PDF downloadLoading ..." @default.
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W2000451798 title "MP41-03 NOTCH SIGNALING PATHWAY AS COMMON TARGET OF ERG IN DIVERSE TUMOR CELL TYPES" @default.
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