Effect of BayK 8644 on [Ca^(2+)]i and Viability in PC3 Human Prostate Cancer Cells

10.4077/CJP.2013.BAB161

Zhen-Rung Lai；Chiang-Ting Chou；Shiuh-Inn Liu；Wei-Zhe Liang；Jong-Khing Huang；Chung-Ren Jan

BayK 8644 ； Ca^(2+) ； PC3

The Chinese Journal of Physiology

56卷6期（2013 / 12 / 31）

318 - 325

英文

The effect of BayK 8644 on cytosolic Ca^(2+) concentrations ([Ca^(2+)]i) and viability in PC3 human prostate cancer cells was explored. Fura-2 was applied to measure [Ca^(2+)]i. BayK 8644 at 1-50 μM induced a [Ca^(2+)]i rise concentration-dependently. The response was reduced by removing extracellular Ca^(2+). BayK 8644-evoked Ca^(2+) entry was inhibited by nifedipine, econazole, SK&F96365, and protein kinase C modulators. In Ca^(2+)-free medium, incubation with the endoplasmic reticulum Ca^(2+) pump inhibitor 2,5-di-tert-butylhydroquinone (BHQ) abolished BayK 8644-induced [Ca^(2+)]i rise. Inhibition of phospholipase C did not alter BayK 8644-induced [Ca^(2+)]i rise. BayK 8644 killed cells in a concentrationdependent manner, which was not reversed by chelating cytosolic Ca^(2+) with 1,2-bis(2-aminophenoxy) ethane-N,N,N',N'-tetraacetic acid/acetoxy methyl (BAPTA/AM). Collectively, in PC3 human prostate cancer cells, BayK 8644 induced a [Ca^(2+)]i rise by evoking phospholipase C-independent Ca^(2+) release from the endoplasmic reticulum and Ca^(2+) entry via protein kinase C-sensitive store-operated Ca^(2+) channels (and/or T-type Ca^(2+) channels). At high concentrations, BayK 8644 caused cell death.

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