BERKELEY, CA (UroToday.com) - The ability to distinguish indolent verses aggressive prostate cancer remains extremely important as prostate tumor metastasis remains the number one cause of death for men with prostate cancer.
The large family of ETS transcription factors are well known for their pro-oncogenic role in many cancer types, especially prostate cancer. ETS transcription factors are often either overexpressed or form oncogeneic fusion proteins which drive prostate tumor progression by upregulating a number of pro-tumorigenic and pro-metastatic genes.
In our study, we summarize the emerging pre-clinical evidence that a new member of the ETS family, PDEF (Prostate-Derived ETS Factor), appears to play an opposite role compared to all the other ETS family members. Increasing amounts of evidence suggest PDEF is a negative regulator of prostate tumor progression through its negative regulation of multiple pro-oncogenic and pro-metastatic genes.
This work builds on our recent finding that PDEF protein levels are decreased even completely lost in aggressive prostate tumors. Our studies have been confirmed and extended by at least two other groups to date. Taken together with other evidence, these studies indicated that loss of PDEF is associated with aggressive tumor behavior, as such PDEF expression could distinguish between indolent and aggressive prostate cancer at the least and PDEF might serve as a novel therapeutic target for castrate resistant prostate cancer, for which we do not have a cure to date.
Clearly PDEF appears to be a prime candidate for further evaluation in prostate cancer.
Written by:
Joshua J. Steffan, Ph.D. and Hari K. Koul, M.Sc., PhD, FACN, FASN. as part of Beyond the Abstract on UroToday.com. This initiative offers a method of publishing for the professional urology community. Authors are given an opportunity to expand on the circumstances, limitations etc... of their research by referencing the published abstract.
Prostate derived ETS factor (PDEF): A putative tumor metastasis suppressor - Abstract
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