Avoiding microRNA Function Through Alternative Polyandenylation in Prostate Cancer.

摘要

Alternative Cleavage and Polyadenylation (APA) is an exciting, yet poorly contributor to tumorigenesis. The current questions that require immediate question are what protein(s) regulate this process and what are the genes most critical that get regulated by this event. Here we tested the hypothesis that APA occurs during acquisition of androgen-independence and the H3K36 trimethylase, Setd2 may modulate this event. While we did not detect any effects to APA due to Setd2, we did determine that the RNA binding protein, CFIm25, is dramatically downregulated in androgen receptor negative prostate cancer cells and that this protein is involved in regulating APA. We used RNA- seq to identify CFIm25 targets and found a significant enrichment in regulated genes that are involved in androgen signaling. These data uncover a previously unknown form of regulation on androgen signaling and give rise to a novel research platform to base future, more substantial research.