Journal
EUROPEAN JOURNAL OF PHARMACOLOGY
Volume 471, Issue 3, Pages 157-164Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/S0014-2999(03)01825-9
Keywords
LNCaP; PC-3; intermediate-conductance K+ channel; intermediate-conducting; Ca2+-activated; riluzole; I-EBIO; benign prostatic hyperplasia
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The effects of 1-ethyl-2-benzimidazolinone (1-EBIO) and riluzole on human prostate cancer cells, LNCaP and PC-3, were evaluated using rubidium (Rb-86(+)) efflux and proliferation assays. 1-EBIO and riluzole evoked concentration-dependent increases in Rb-86(+) efflux from LNCaP and PC-3 cells that were sensitive to inhibition by intermediate-conductance Ca2+-activated K+ channel (IKCa) blockers clotrimazole and charybdotoxin. Blockers of large-conductance Ca2+-activated K+ (IKCa) channel, iberiotoxin, or small-conductance Ca2+-activated K+ (SKCa) channel, apamin or scyllatoxin, had no effect. Concurrently, both 1-EBIO and riluzole evoked concentration-dependent increases in proliferation from human prostate cancer cell lines (LNCaP and PC-3 cells). Clotrimazole and charybdotoxin, but not iberiotoxin, apamin or scyllatoxin, inhibited 1-EBIO- and ffluzole-evoked increases in proliferation from LNCaP and PC-3 cells. N-(3-(trifluoromethyl)phenyl)-N'-(2-hydroxy-5-chlorophenyl)urea (NS-1608) and 2-amino-5-(2-fluorophenyl)-4-methyl-1H-pyrrole-3-carbonitrile (NS-8), BKCa channel openers had no effect on LNCaP and PC-3 proliferation. These results demonstrate that IKCa channels play an important role in the regulation of human prostate cancer cell proliferation. (C) 2003 Elsevier Science B.V. All rights reserved.
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