The influence of peptides from the angiotensin family on tyrosine kinase activity and cell viability in a human hormone-dependent prostate cancer line.

The results of many studies have reported that peptides from the angiotensin family are involved in the regulation of cell growth, proliferation, cell migration, apoptosis, inflammation, differentiation, and angiogenesis, which suggests that they might play an important role in carcinogenesis. The role of the renin-angiotensin system in supporting prostate cancer induction and progression has so far received little study. The present study was to examine the influence of Ang II, Ang III, and Ang IV on a human hormone-dependent prostate cancer line (LNCaP). Using an isotopic method, we tested the effects of angiotensins on tyrosine kinase activity, and measured cell viability using an MTT Assay. The results showed that only Ang IV significantly reduced tyrosine kinase activity and cell viability in LNCaP cells. The process seemed to be mediated partly by AT(2) and probably by another type of receptor with high affinity for Ang IV and low affinity for PD123319 and Losartan. These findings suggest that components of the renin-angiotensin system, specifically angiotensin peptides and receptors (AT(1), AT(2)) can modify prostate cancer cell viability.