Beta-catenin is elevated in human benign prostatic hyperplasia specimens compared to histologically normal prostate...

Area of Science:

• Urology
• Molecular Biology
• Cell Biology

Background:

• Benign prostatic hyperplasia (BPH) is a common condition causing lower urinary tract symptoms (LUTS).
• The underlying molecular mechanisms driving BPH pathogenesis remain incompletely understood.
• Beta-catenin (CTNNB1) signaling is implicated in various cellular processes and diseases.

Purpose of the Study:

• To investigate differences in beta-catenin (CTNNB1) immunostaining intensity and distribution in human BPH tissue compared to normal prostate tissue.
• To examine the expression of CTNNB1's putative target gene, lymphoid enhancer binding factor 1 (LEF1), in BPH.
• To correlate CTNNB1 and LEF1 expression patterns with BPH histology.

Main Methods:

• Multiplex immunostaining was performed on human prostate tissue specimens with and without BPH.
• Proteins analyzed included CTNNB1, LEF1, and the epithelial marker E-cadherin.
• Quantification of staining intensity, cellular localization (membranous, cytoplasmic, nuclear), and tissue distribution (stromal, epithelial) was conducted using multispectral imaging.

Main Results:

• CTNNB1 staining intensity was significantly higher in BPH tissues, particularly in stromal cell membranes, cytoplasm, nuclei, and epithelial cell nuclei.
• LEF1 staining intensity and the percentage of LEF1-positive stromal cells were significantly lower in BPH tissues.
• Specific patterns of CTNNB1 and LEF1 nuclear co-expression differed between BPH and normal prostate tissues.

Conclusions:

• The findings support the hypothesis that CTNNB1 expression is increased in specific compartments within BPH tissues.
• Nuclear LEF1 staining did not consistently correlate with CTNNB1 staining, suggesting it may not be a reliable indicator of CTNNB1 activity in the prostate.
• These results provide insights into the molecular alterations in BPH and potential roles of CTNNB1 signaling.