Finasteride targets prostate vascularity by inducing apoptosis and inhibiting cell adhesion of benign and malignant prostate cells
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Updated: Aug 9, 2026

Murine Prostate Micro-dissection and Surgical Castration
Published on: May 11, 2016
M Tandy Sutton1, Melissa Yingling, Ash Vyas
1Division of Urology, University of Kentucky Medical Center, 800 Rose Street, Lexington, KY 40536, USA.
Background:
This study investigated the effects of finasteride, a 5alpha-reductase inhibitor, clinically used for the treatment of benign prostatic hyperplasia (BPH) on prostate tumor vascularity, apoptosis, and cell adhesion in situ and in vitro.
Methods:
Prostate specimens from BPH patients treated with finasteride for 1-12 months (n = 13), or without finasteride treatment (n = 14), were evaluated for apoptosis (TUNEL assay), microvessel density (Factor VIII), and prostate specific antigen (PSA) immunoreactivity. In vitro, the effect of finasteride was investigated in benign prostate cells, BPH-1, and its tumorigenic derivatives, CAFTD-01 and CAFTD-03, using Hoechst staining and cell adhesion assays.
Results:
A significant increase in the apoptotic index, and reduced microvessel density and PSA expression were detected in prostates from finasteride-treated patients, compared to controls (P < 0.01). In vitro finasteride led to a significant decrease in prostate epithelial cell adhesion (P < 0.05).
Conclusions:
Finasteride can induce prostate apoptosis and reduce tissue vascularity by inhibiting epithelial cell adhesion. This evidence supports that finasteride has apoptotic and anti-angiogenic effects against benign and malignant prostate.
Insights
Finasteride, used for benign prostatic hyperplasia (BPH), significantly increases prostate apoptosis and reduces vascularity by inhibiting cell adhesion. This suggests finasteride offers both apoptotic and anti-angiogenic benefits for prostate conditions.
Area of Science:
- Urology
- Oncology
- Pharmacology
Background:
- Finasteride is a 5alpha-reductase inhibitor used for benign prostatic hyperplasia (BPH).
- Investigated finasteride's effects on prostate tumor vascularity, apoptosis, and cell adhesion.
- Evaluated effects both in vivo (patients) and in vitro (cell lines).
Purpose of the Study:
- To determine the impact of finasteride on prostate apoptosis.
- To assess finasteride's effect on prostate tumor vascularity.
- To investigate finasteride's influence on prostate epithelial cell adhesion.
Main Methods:
- Analyzed prostate specimens from BPH patients with and without finasteride treatment.
- Assessed apoptosis using TUNEL assay and microvessel density via Factor VIII staining.
- Utilized Hoechst staining and cell adhesion assays in vitro with BPH and prostate cancer cell lines.
Main Results:
- Finasteride treatment significantly increased the apoptotic index in patient prostates.
- Reduced microvessel density and prostate-specific antigen (PSA) expression were observed in treated patients.
- In vitro, finasteride significantly decreased prostate epithelial cell adhesion.
Conclusions:
- Finasteride demonstrates apoptotic and anti-angiogenic effects in prostate tissues.
- Inhibition of epithelial cell adhesion is a key mechanism for finasteride's effects.
- Findings support finasteride's potential therapeutic role in benign and malignant prostate conditions.
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