Roles of NF-κB activation in benign prostatic hyperplasia and association between NF-κB and HIF-1α

Area of Science:

• Urology
• Molecular Biology
• Pathology

Background:

• Benign prostatic hyperplasia (BPH) is a common condition in aging men.
• The role of inflammatory pathways, such as Nuclear Factor-kappa B (NF-κB), in BPH pathogenesis is not fully understood.
• Understanding molecular drivers is crucial for BPH management.

Purpose of the Study:

• To investigate the expression and role of NF-κB activation in human BPH tissues.
• To correlate NF-κB expression with clinical parameters, hormone receptors, and hypoxia-inducible factor 1-alpha (HIF-1α).

Main Methods:

• Immunohistochemistry was used to detect NF-κB expression in 101 BPH tissue samples.
• Expression was analyzed in both glandular and stromal compartments.
• Correlations with clinical data, hormone receptors (androgen, progesterone), HIF-1α, and microvessel density were evaluated.

Main Results:

• NF-κB expression was detected in 37.6% of glands and 30.7% of stroma.
• Stromal NF-κB activation significantly correlated with lower total and T-zone prostate volumes.
• No significant correlation was found between stromal NF-κB and HIF-1α or microvessel density.
• Stromal androgen and progesterone receptor expression was higher in HIF-1α negative cases.
• Diffuse fibrosis was more frequent in NF-κB inactivated, HIF-1α positive cases.

Conclusions:

• Stromal NF-κB activation is associated with reduced prostate size in BPH patients.
• NF-κB inactivation combined with HIF-1α positivity may indicate increased susceptibility to diffuse fibrosis in BPH.