Finasteride targets prostate vascularity by inducing apoptosis and inhibiting cell adhesion of benign and malignant prostate cells

M. Tandy Sutton, Melissa Yingling, Ash Vyas, Humphrey Atiemo, Andrew Borkowski, Stephen C. Jacobs, Natasha Kyprianou

Research output: Contribution to journalArticlepeer-review

20 Scopus citations

Abstract

BACKGROUND. This study investigated the effects of finasteride, a 5α-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.

Original languageEnglish
Pages (from-to)1194-1202
Number of pages9
JournalProstate
Volume66
Issue number11
DOIs
StatePublished - 1 Aug 2006
Externally publishedYes

Keywords

  • Apoptosis
  • Cell adhesion
  • Finasteride
  • Prostate cells
  • Vascularity

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