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Evaluation of role of angiotensin III and aminopeptidases in prostate cancer cells
Author(s) -
Teranishi Junichi,
Ishiguro Hitoshi,
Hoshino Koji,
Noguchi Kazumi,
Kubota Yoshinobu,
Uemura Hiroji
Publication year - 2008
Publication title -
the prostate
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.295
H-Index - 123
eISSN - 1097-0045
pISSN - 0270-4137
DOI - 10.1002/pros.20835
Subject(s) - lncap , prostate cancer , prostate , endocrinology , cancer research , medicine , angiotensin ii , cell growth , olmesartan , cancer , cancer cell , biology , receptor , biochemistry , blood pressure
BACKGROUND The aim of this study was to perform a comprehensive evaluation of angiotensin III (Ang‐III) and related converting enzymes, aminopeptidase A (APA) and N (APN), in prostate cancer. METHODS We investigated the effects of Ang‐III on the in vitro growth of human prostate cancer cells and the expression of APA and APN in cells treated with Ang‐III or hormonal agents. Furthermore, we performed real‐time quantitative PCR to investigate the expression pattern of APA and APN in 86 prostate tissue samples including normal prostate, untreated and hormone refractory prostate cancer (HRPC). RESULTS Ang‐III stimulated cell proliferation, and the proliferative effect was inhibited by olmesartan, an AT 1 receptor blocker (ARB). Western blot analysis showed that phosphorylation of mitogen‐activated protein kinase (MAPK) was enhanced by Ang‐III and inhibited by olmesartan. APN mRNA level in HRPC was significantly lower than that in normal prostate and untreated prostate cancer tissue. In LNCaP cells, APN expression was augmented by Ang‐III, whereas APA expression was not modulated. Hormonal agents, such as estradiol (E2) and dexamethasone (Dex), enhanced APA expression, but did not modulate APN expression in LNCaP cells. CONCLUSIONS Our results suggest that Ang‐III and related converting enzymes contribute to cell proliferation of prostate cancer, and may be implicated in cancer progression. Prostate 68: 1666–1673, 2008. © 2008 Wiley‐Liss, Inc.