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Calcium signaling in prostate cancer cells: Evidence for multiple receptors and enhanced sensitivity to bombesin/GRP
Author(s) -
Wasilenko William J.,
Cooper Jeffrey,
Palad Ann J.,
Somers Kenneth D.,
Blackmore Peter F.,
Rhim Johng S.,
Wright George L.,
Schellhammer Paul F.
Publication year - 1997
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/(sici)1097-0045(19970215)30:3<167::aid-pros4>3.0.co;2-j
Subject(s) - bombesin , prostate cancer , receptor , prostate , endocrinology , medicine , calcium , signal transduction , cancer research , calcium signaling , cancer , biology , microbiology and biotechnology , neuropeptide
BACKGROUND Cellular calcium is an important second messenger for growth regulation. We sought to identify potentially important receptors on prostate tumor cells by screening over 20 agonists for their ability to increase intracellular free calcium ([Ca 2+ ] i ) in several human prostate tumor cell lines. METHODS Intracellular calcium mobilization was detected using fura‐2. RESULTS We found bombesin, GRP, ATP/UTP, lysophosphatidic acid, thrombin, endothelin, histamine, and bradykinin increased [Ca 2+ ] i in the advanced tumor cell lines DU‐145, PC3, and PPC‐1. Bombesin failed to elevate [Ca 2+ ] i in an immortalized human prostate cell line. Rank‐order of potency studies suggested the presence of P 2U nucleotide receptors for ATP/UTP on prostate epithelial cells. Potency studies also revealed GRP>>bombesin>>neuromedin B at elevating [Ca 2+ ] i in responding tumor cells. CONCLUSIONS These findings indicate that androgen independent prostate tumor cell lines express multiple receptors capable of elevating intracellular calcium, and suggest that GRP receptors may be selectively expressed and/or coupled to calcium signaling during prostate tumor progression. Calcium sensitive cellular events may therefore contribute to the progression of prostate cancer. Prostate 30:167–173, 1997 . © 1997 Wiley‐Liss, Inc.