Angiotensin receptors in hormone-independent prostate cancer cell line DU145: Presence of two variants of angiotensin type 1 receptor
Małgorzata Sidorkiewicz, Elżbieta Rebas, Marta Szymajda, Hanna Lawnicka, Marek Pawlikowski, Agnieszka Lachowicz
Department of Medical Biochemistry, Medical University of Łódź, Łódź, Poland
Med Sci Monit 2009; 15(4): BR106-110
Background: Recently, the involvement of the renin-angiotensin system in the proliferation of prostate cancer has been suggested. There is increasing evidence that angiotensin II receptor type 1 (AT1) is expressed in a variety of cancer cells and tissues and may have a role in tumor growth, angiogenesis, and invasive activity of malignant lesions in vivo. The implications of data referring to an angiotensin receptor in hormone-independent human prostate cancer DU145 cells are unclear. Angiotensin II has been shown to inhibit the proliferation of DU145 cell lines. However, it is known that AT1 stimulates cell proliferation and that angiotensin II receptor type 2 (AT2) induces apoptosis and inhibits cell proliferation.
Material/Methods: The aim of our study was to investigate, by means of immunohistochemical and reverse transcriptase polymerase chain reaction assays, the type of angiotensin II receptor that is present in DU145 cells.
Results: In DU145-derived complementary deoxyribonucleic acid (cDNA), a polymerase chain reaction assay revealed 2 AT1-specific PCR products (93 bp and 126 bp). DU145-derived cDNA did not reveal AT2 expression at a level sufficient for detection by PCR. In cultured cells, immunohistochemical testing revealed a positive reaction in cultures immunostained with anti-AT1 antibody but not in those immunostained with AT2 antibody.
Conclusions: The inhibitory effect of angiotensin II on the proliferation of DU145 cells is exerted via AT1. It is possible that presence of 2 variants of AT1 in that cancer cell line is essential to produce the biological effects of angiotensin
Keywords: Angiotensin II, DU-145, human prostate cancer, Base Sequence, Cell Line, Tumor, DNA Primers, DNA, Complementary, Prostatic Neoplasms - pathology, Receptor, Angiotensin, Type 1 - metabolism, Reverse Transcriptase Polymerase Chain Reaction