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Prostate cancer is the most common non-dermatologic malignancy in men in the Western world. Recently, a frequent chromosomal aberration fusing androgen regulated  TMPRSS2  promoter and the  ERG  gene ( TMPRSS2/ERG ) was discovered in prostate cancer. Several studies demonstrated cooperation between  TMPRSS2/ERG  and other defective pathways in cancer progression. However, the unveiling of more specific pathways in which  TMPRSS2/ERG  takes part, requires further investigation. Using immortalized prostate epithelial cells we were able to show that  TMPRSS2/ERG  over-expressing cells undergo an Epithelial to Mesenchymal Transition (EMT), manifested by acquisition of mesenchymal morphology and markers as well as migration and invasion capabilities. These findings were corroborated  in vivo , where the control cells gave rise to discrete nodules while the  TMPRSS2/ERG -expressing cells formed malignant tumors, which expressed EMT markers. To further investigate the general transcription scheme induced by  TMPRSS2/ERG , cells were subjected to a microarray analysis that revealed a distinct EMT expression program, including up-regulation of the EMT facilitators,  ZEB1  and  ZEB2,  and down-regulation of the epithelial marker  CDH1 (E-Cadherin). A chromatin immunoprecipitation assay revealed direct binding of  TMPRSS2/ERG  to the promoter of  ZEB1  but not  ZEB2 . However,  TMPRSS2/ERG  was able to bind the promoters of the  ZEB2  modulators,  IL1R2  and  SPINT1 . This set of experiments further illuminates the mechanism by which the  TMPRSS2/ERG  fusion affects prostate cancer progression and might assist in targeting  TMPRSS2/ERG  and its downstream targets in future drug design efforts.

TMPRSS2/ERG Promotes Epithelial to Mesenchymal Transition through the ZEB1/ZEB2 Axis in a Prostate Cancer Model