The spliceosome as a new therapeutic vulnerability in aggressive prostate cancer.

Abstract

Alternative splicing (AS) analysis across the entire spectrum of human prostate cancer evolution reveals the unexpected findings that intron retention is a hallmark of stemness and tumor aggressiveness, and androgen receptor controls a splicing program distinct from its transcriptional regulation. Importantly, twisted activity of the spliceosome causing abnormal AS landscape represents a therapeutic vulnerability in aggressive prostate cancer.