Inhibiting CBP Decreases AR Expression and Inhibits Proliferation in Benign Prostate Epithelial Cells

Area of Science:

• Urology
• Molecular Biology
• Cell Biology

Background:

• CREB-binding protein (CBP) acts as a crucial transcriptional coactivator for androgen receptors (AR).
• Understanding CBP's role in AR regulation is vital for benign prostatic hyperplasia (BPH) research.

Purpose of the Study:

• To investigate the impact of CBP on AR expression and prostate epithelial cell proliferation in BPH.
• To explore CBP as a potential therapeutic target for BPH.

Main Methods:

• Analysis of a published dataset and BPH patient tissues to assess CBP and AR expression.
• Inhibition of CBP using ICG-001 and shRNA in BPH-1 and RWPE-1 cells.
• Utilized immunofluorescence, cell viability assays, flow cytometry, Western blot, and co-immunoprecipitation to analyze CBP's effects and interaction with AR.

Main Results:

• CBP expression correlates with AR expression in prostate tissues.
• CBP inhibition led to decreased AR expression, reduced proliferation, induced apoptosis, and cell cycle arrest in BPH cells.
• Co-immunoprecipitation confirmed that CBP binds to AR, forming transcription complexes.

Conclusions:

• Inhibiting CBP effectively reduces AR expression and suppresses proliferation in benign prostate epithelial cells.
• CBP presents a promising therapeutic target for modulating AR expression and proliferation in BPH.