VIP and PACAP are autocrine factors that protect the androgen‐independent prostate cancer cell line PC‐3 from apoptosis induced by serum withdrawal
作者： Irene Gutiérrez‐Cañas , Nieves Rodríguez‐Henche , Oscar Bolaños , María J Carmena , Juan C Prieto
关键词: Receptor 、 Vasoactive intestinal peptide 、 Autocrine signalling 、 Molecular biology 、 Apoptosis 、 Receptor antagonist 、 Paracrine signalling 、 Biology 、 Agonist 、 Endocrinology 、 Cell culture 、 Internal medicine
摘要: 1. In the present study, we describe expression of neuropeptides vasoactive intestinal peptide (VIP) and pituitary adenylate cyclase-activating polypeptide (PACAP) as well their receptors in PC-3 cells, a human prostate cancer cell line. addition, have investigated role apoptosis induced by serum starvation. 2. By RT-PCR immunocytochemistry assays, demonstrated production VIP PACAP cells. 3. We binding assays common PACAP/VIP (VPAC(1) VPAC(2)) receptors, but not PACAP-specific (PAC(1)) receptors. The pharmacological profile [(125)I]-VIP was follows: VPAC(1) antagonist=VPAC(1) agonist>VIP>VPAC(2) agonist (IC(50)=1.2, 1.5, 2.3 30 nM, respectively). both receptor subtypes are functional since VIP, PACAP-27 or VPAC(2) agonists all increased intracellular levels cAMP. 4. peptides is similar serum-cultured serum-deprived treatment cells with exogenous increases number viability dose-dependent manner, cellular counting MTT assays. survival exerted through receptor, VPAC(1), VPAC(2), agonist, mimics effects antagonist blocks it. Moreover, inhibit genomic DNA fragmentation triggered starvation, increase immunoreactivity antiapoptotic protein bcl-2. 5. Our results suggest that autocrine/paracrine factors protect from VPAC1
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