LincRNAs and AR Reactivation after Androgen Deprivation in Prostate Cancer Cells
Final rept. 30 Sep 2013-29 Sep 2014
CREIGHTON UNIV OMAHA NE
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Prostate cancer PCa represents the most frequently diagnosed malignancy of men in the US. Reactivation of androgen receptor AR signaling following androgen deprivation is a major driver of the development of castration-resistant prostate cancer CRPC. Understanding the precise mechanisms underlying aberrant AR-regulated gene activation will advance our knowledge of PCa tumorigenesis, with implementation of new therapeutic strategies. LincRNAs are recently identified novel genetic materials. The role of linRNAs in cancer is being increasingly accepted, both as possible specific biomarkers and as potential therapeutic targets. However, how aberrant expression of these lincRNAs contributes to PCa progression is still not fully understood. This one-year hypothesis-exploratory project was designed to test a novel hypothesis that lincRNAs promote AR reactivation in prostate cancer cells following androgen deprivation through modulation of AREZH2-mediated repressive chromatin remodeling. The experiments as proposed were successfully completed during the funding peroid and objectives achieved. Resultant data provide a basis for the identification of novel targets for therapeutic intervention for PCa. The ultimate goal is to define the molecular mechanisms of PCa initiation and development and to develop effective treatments.
- Anatomy and Physiology
- Medicine and Medical Research