Interrogating The Mechanism Of Long Noncoding RNA ARlnc-1 In Regulating AR Signaling
Abstract
Prostate cancer is the most commonly diagnosed type of non-skin cancer in American men. It is estimated that ~164,690 new cases will be diagnosed in 2018. Despite the fact that most patients with primary prostate cancer can be cured with androgen deprivation therapy (ADT), in some patients, disease progresses to metastasis state, which is castration-resistant and always lethal. Researchers have been searching for the molecular mechanisms that contribute to the progression of castration resistant prostate cancer (CRPC). One of the mechanisms highlights the continued activation of AR signaling, for example, by AR gene amplification, splicing variants of AR transcript, as well as promiscuous activation of AR. Most of these studies focused on investigating protein-coding genes, meanwhile, the study of lncRNAs associated with AR signaling is lacking. To fulfill this knowledge gap, out lab previously conducted a comprehensive profiling of androgen regulated non-coding transcriptome in cell lines and patient samples. In an effort to identify lncRNAs that are both induced by androgen stimulation, and have elevated expression in primary and metastasis prostate cancer (compared to normal prostate), we discovered a top candidate, ARlnc1. Expression of this lncRNA is highly prostate-lineage specific, driven by AR and FOXA1.
Document Details
- Document Type
- Technical Report
- Publication Date
- May 01, 2018
- Accession Number
- AD1056605
Entities
People
- Yajia Zhang
Organizations
- University of Michigan