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Introduction: 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., Material and Methods: 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., Results: 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., Conclusions: 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.

Angiotensin III is the biological active peptide from the angiotensin family, which play the important role in several cellular processes. Ang III is the product of reaction catalyzed by aminopeptidase A and in turn can be a substrate for aminopeptidase N, enzyme which converts Ang III to shorter fragment, Ang IV. Aminopeptidase N is specifically inhibited by PC18. Ang III can act by binding to receptors AT1, AT2 or other type of receptors, which are not well recognized. The connection of Ang III to AT1 and AT2 receptors could be inhibited by losartan or PD123319, respectively. The aim of this study was to investigate what is the influence of angiotensin III on protein tyrosine kinase activity in rat pituitary and what is the possible place of interaction of Ang III with target cells. The obtained results show that Ang III can modify tyrosine kinase activity in concentration dependent manner but Ang IV appeared more effective. In presence of PC18 Ang III caused the same changes as Ang III alone that suggests that Ang III, not its metabolite modify tyrosine kinase activity. Losartan and PD123319 given together with Ang III enhanced the changes induced by Ang III. It suggests that the investigated peptide has an effect on protein tyrosine kinase activity in a different way than via AT1 and AT2 receptors.