L K Chopin1, A C Herington. 1. Centre for Molecular Biotechnology, School of Life Sciences, Queensland University of Technology, Brisbane, Queensland, Australia. l.chopin@qut.edu.au
Abstract
BACKGROUND: Recent studies have shown that GHRH antagonists inhibit prostate tumour growth and IGF-II production both in vivo and in vitro. The mechanism underlying these observations is unknown, but may involve an interaction with a prostatic GHRH receptor (GHRH-R), raising the possibility of an autocrine pathway for the GHRH axis in the prostate. METHODS: GHRH and GHRH-R mRNA expression was examined by RT-PCR in human prostate cancer cell lines, and the authenticity of PCR products was confirmed by Southern analysis and cDNA sequencing. Immunohistochemical techniques were used to examine the expression of GHRH protein in prostate cancer cell lines. RESULTS: GHRH-R (mRNA) and GHRH (mRNA and protein) are co-expressed in the ALVA-41, DU145, LNCaP and PC3 human prostate cancer cell lines. CONCLUSIONS: These observations suggest the presence of an intact prostatic GHRH autocrine pathway which may stimulate prostate cell proliferation. This pathway may be disrupted by GHRH antagonists. Copyright 2001 Wiley-Liss, Inc.
BACKGROUND: Recent studies have shown that GHRH antagonists inhibit prostate tumour growth and IGF-II production both in vivo and in vitro. The mechanism underlying these observations is unknown, but may involve an interaction with a prostatic GHRH receptor (GHRH-R), raising the possibility of an autocrine pathway for the GHRH axis in the prostate. METHODS:GHRH and GHRH-R mRNA expression was examined by RT-PCR in humanprostate cancer cell lines, and the authenticity of PCR products was confirmed by Southern analysis and cDNA sequencing. Immunohistochemical techniques were used to examine the expression of GHRH protein in prostate cancer cell lines. RESULTS:GHRH-R (mRNA) and GHRH (mRNA and protein) are co-expressed in the ALVA-41, DU145, LNCaP and PC3humanprostate cancer cell lines. CONCLUSIONS: These observations suggest the presence of an intact prostatic GHRH autocrine pathway which may stimulate prostate cell proliferation. This pathway may be disrupted by GHRH antagonists. Copyright 2001 Wiley-Liss, Inc.
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