Program in Urosciences, Division of Urology, Department of Surgery, University of Colorado, Denver.
School of Medicine, Building P15 or RC2, MS: C317, 12700 E 19th Avenue, Aurora, CO 80045, USA; Denver Veterans Administrative Medical Center, 1055 Clermont St. Denver, CO 80220, USA; University of Colorado Comprehensive Cancer Center, Building P15 or RC2, MS: C317, 12700 E 19th Avenue, Aurora, CO 80045, USA.
The prostate-derived ETS factor (PDEF) is the latest family member of the ETS transcription factor family, although it is unique in many aspects. PDEF was first described as an mRNA transcript highly expressed in prostate tumor cells where it regulates prostate-specific antigen gene expression and is an androgen receptor co-regulator. PDEF expression is highly restricted to epithelial cells and has only been found in prostate, breast, colon, ovary, gastric, and airway epithelium. Strong preclinical evidence is emerging that PDEF is a negative regulator of tumor progression and metastasis. PDEF expression is often lost in late-stage, advanced tumors. The induction of tumor aggressiveness in response to the loss of PDEF is thought to be due to the plethora of PDEF-regulated gene targets, many of which are known players in tumor progression including tumor cell invasion and metastasis. These data have lead to the hypothesis that PDEF may function as a tumor metastasis suppressor. In this review, we summarize what is known about PDEF since its discovery over a decade ago and give a detailed overview of PDEF-regulated gene products and the expression profiles of PDEF in clinical tumor samples.
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Steffan JJ, Koul HK. Are you the author?
Reference: Cancer Lett. 2011 Jun 29. Epub ahead of print.
doi: 10.1016/j.canlet.2011.06.011
PubMed Abstract
PMID: 21764212
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