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Research Article Free access | 10.1172/JCI115562

P2-purinergic receptor agonists inhibit the growth of androgen-independent prostate carcinoma cells.

W G Fang, F Pirnia, Y J Bang, C E Myers, and J B Trepel

Clinical Pharmacology Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892.

Find articles by Fang, W. in: PubMed | Google Scholar

Clinical Pharmacology Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892.

Find articles by Pirnia, F. in: PubMed | Google Scholar

Clinical Pharmacology Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892.

Find articles by Bang, Y. in: PubMed | Google Scholar

Clinical Pharmacology Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892.

Find articles by Myers, C. in: PubMed | Google Scholar

Clinical Pharmacology Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892.

Find articles by Trepel, J. in: PubMed | Google Scholar

Published January 1, 1992 - More info

Published in Volume 89, Issue 1 on January 1, 1992
J Clin Invest. 1992;89(1):191–196. https://doi.org/10.1172/JCI115562.
© 1992 The American Society for Clinical Investigation
Published January 1, 1992 - Version history
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Abstract

To develop a new approach to the treatment of advanced, hormone-refractory prostate cancer, the signal transductions regulating the growth of human androgen-independent prostate carcinoma cell lines were studied. Agonist-stimulated Ca2+ mobilization, a critical regulatory event in other secretory cell types, was studied as a means of identifying previously undescribed plasma membrane receptors that may transduce a growth inhibitory signal. In all of the cell lines tested, P2-purinergic receptor agonists, including ATP and certain hydrolysis-resistant adenine nucleotides, induced a rapid, transient increase in cytoplasmic free Ca2+ that was detectable at 50 to 100 nM ATP, was maximal at 100 microM ATP, and was inhibited approximately 50% by chelation of extracellular Ca2+. Within 8 s after addition, ATP stimulated accumulation of the polyphosphatidylinositol products inositol (1, 4, 5) trisphosphate, inositol (1, 3, 4) trisphosphate, and inositol tetrakisphosphate. In addition to stimulating phosphatidylinositol turnover and Ca2+ mobilization, ATP and hydrolysis-resistant ATP analogues induced greater than 90% inhibition of the growth of all lines tested. These data demonstrate that human androgen-independent prostate carcinoma cells express functional P2-purinergic receptors linked to phospholipase C, and that agonists of this receptor are markedly growth inhibitory, suggesting a novel therapeutic approach to this common adult neoplasm.

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