Amplification of the urokinase gene and the sensitivity of prostate cancer cells to urokinase inhibitors

BJU Int. 2006 Feb;97(2):404-9. doi: 10.1111/j.1464-410X.2005.05912.x.

Abstract

Objectives: To evaluate the frequency of the urokinase-type plasminogen activator (uPA) gene amplification and the sensitivity of prostate cancer cells to uPA inhibition, as we previously found one hormone-refractory prostate tumour with high-level amplification of the uPA (alias PLAU) gene, and also showed that a uPA inhibitor, amiloride, can effectively reduce the invasion potential of the PC-3 prostate cancer cell line.

Materials and methods: Sixty-three locally recurrent hormone-refractory tumours and 78 hormone-refractory metastases from 29 patients who died from prostate cancer were analysed for uPA gene-copy number using fluorescence in situ hybridization. The Matrigel invasion assay was used to study the influence of uPA inhibitors on the invasive potential of prostate cancer cell lines.

Results: Of the locally recurrent hormone-refractory tumours, 21% had an increased copy number of uPA, but no high-level amplifications were found; 31% of the metastases had increased copy number and one high-level amplification of the uPA. Matrigel invasion assays with two specific uPA inhibitors, B428 and p-aminobenzamidine, showed that invasion of a prostate cancer cell line containing uPA gene amplification was inhibited by these small-molecule uPA inhibitors, while invasion of prostate cell lines without uPA gene amplification were not.

Conclusion: These results suggest that selective inhibition of the uPA pathway in individuals whose tumours contain uPA gene amplification may provide therapeutic benefit.

Publication types

  • Evaluation Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Amiloride / therapeutic use*
  • Blood Proteins / therapeutic use*
  • Gene Amplification / genetics
  • Humans
  • In Situ Hybridization, Fluorescence / methods
  • Male
  • Neoplasm Recurrence, Local / drug therapy
  • Neoplasm Recurrence, Local / genetics
  • Neoplasms, Hormone-Dependent / drug therapy
  • Neoplasms, Hormone-Dependent / genetics*
  • Prostatic Neoplasms / drug therapy
  • Prostatic Neoplasms / genetics*
  • Reverse Transcriptase Polymerase Chain Reaction / methods
  • Sensitivity and Specificity
  • Urokinase-Type Plasminogen Activator / genetics*

Substances

  • Blood Proteins
  • urokinase inhibitor
  • Amiloride
  • Urokinase-Type Plasminogen Activator