Endopeptidase 24.11 activity in the human prostate cancer cell lines LNCaP and PPC-1

A. Krongrad, Elena Nikolaevna Atochina, J. V V Ryan, B. A. Roos

Research output: Contribution to journalArticle

4 Citations (Scopus)

Abstract

Human endopeptidase 24.11 (EP) occurs in greatest abundance on terminally differentiated prostate cells; thus, loss of EP could mark dedifferentiation of prostate epithelium. To identify laboratory models that would permit continuous work oil the biochemistry and hormonal regulation of EP, we examined the well differentiated LNCaP and poorly differentiated PPC-1 human prostate cancer cell lines. Ultrastructural analysis revealed that LNCaP secretes electron-dense material that resembles the particulate matter of seminal plasma, which is associated with endopeptidase activity. LNCaP medium contained EP activity while PPC-1 medium did not. Whether the apparent deletion of EP from the PPC-1 cell line is characteristic of poorly differentiated prostate adenocarcinoma is not yet clear. However, it may be relevant to the carcinogenic process that EP can limit growth of lung small carcinomas by inactivating cell growth-promoting bombesin-like peptides. Because bombesin has been identified in aggressive human prostate cancers, loss of EP in PPC-1 could represent a necessary step in transformation to aggressive phenotype. The combination of LNCaP and PPC-1, which offers well-differentiated and poorly differentiated cancer phenotypes, appears well suited to studying the relevance of EP in prostate cancer biology.

Original languageEnglish
Pages (from-to)113-116
Number of pages4
JournalUrological Research
Volume25
Issue number2
DOIs
Publication statusPublished - Apr 1997
Externally publishedYes

Keywords

  • Endopeptidase 24.11
  • Growth
  • LNCaP
  • PPC-1
  • Prostate cancer

ASJC Scopus subject areas

  • Urology

Fingerprint Dive into the research topics of 'Endopeptidase 24.11 activity in the human prostate cancer cell lines LNCaP and PPC-1'. Together they form a unique fingerprint.

  • Cite this