Prostate cancer (PCa) represents the most frequently diagnosed malignancy of men in the United States, with a lifetime incidence risk of 1 in 6, and an expected 241,000 new cases and 33,700 deaths in 2011. The androgen receptor (AR) is a member of a nuclear receptor superfamily that regulates gene transcription. Many of these AR-regulated genes are key regulators to prostate development and progression. 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 human genome encodes thousands of lincRNAs and each of these molecules can control hundreds of genes. Therefore, these molecules are extremely powerful molecules that regulate almost all aspects of the host's well-being. Recent research indicates that many lincRNAs have been linked to the initiation and progression of human cancer. The role of linRNAs in cancer is being increasingly accepted, both as possible specific biomarkers and as potential therapeutic targets. LincRNA expression becomes altered with the development and progression of PCa. However, how aberrant expression of these lincRNAs contributes to PCa progression is still not fully understood. This proposal will address the overarching challenge to elucidate the role of lincRNAs in AR-regulated gene activation in PCa. Resultant data should 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 for this critically important disease.
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