Canonical androgen response element motifs are tumor suppressive regulatory elements in the prostate.

ABSTRACT: The androgen receptor (AR) is central in prostate tissue identity and differentiation, and controls normal growth-suppressive, prostate-specific gene expression. It also drives prostate tumorigenesis when hijacked for oncogenic transcription. The execution of growth-suppressive AR transcriptional programs in prostate cancer (PCa) and the potential for reactivation remain unclear. Here, we use a genome-wide approach to modulate canonical androgen response element (ARE) motifs-the classic DNA binding elements for AR-to delineate distinct AR transcriptional programs. We find that activating these AREs promotes differentiation and growth-suppressive transcription, potentially leading to AR⁺ PCa cell death, while ARE repression is tolerated by PCa cells but deleterious to normal pros

SUBMITTER: Chen X 

PROVIDER: S-EPMC11645413 | biostudies-literature | 2024 Dec

REPOSITORIES: biostudies-literature