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- W111918674 abstract "We have reported that both incidence and mortality of prostate cancer (PC) are decreased in a dose dependent manner by boron in diet (Oncology Rep 2004) and drinking water (Cancer Causes Control 2007). Boric acid (BA) inhibits PC cell proliferation (Cancer Lt 2004), binds to NAD+ and inhibits ADP ribosyl cyclase (J Mass Spec 2003,2004; J Chromatography 2006). Our present objective was to determine BA's effect on Ca2+ store release in DU-145 cells. Endoplasmic reticulum (ER) Ca2+ was labeled with Rhod 2 and Ca2+ release was monitored using a Zeiss LSM 5 Pascal laser confocal microscope. BA inhibited Ca2+ release in response to 10 ìM cyclopiazonic acid (SERCA inhibitor) and 20 mM caffeine (ryanodine channel agonist) in a dose dependent manner beginning at 0.1 ìM BA. BA inhibited Ca2+ release in response to 4-chloro-m-cresol in a dose dependent manner from 0.1 ìM BA to near complete inhibition at 10 ìM BA. Inhibition of caffeine induced Ca2+ release required >10 fold higher concentrations BA (150 ìM) in PWR1E non-tumor cells than DU-145 tumor cells. Our results demonstrate that BA acts as a ryanodine receptor antagonist and suggests boron's chemopreventative effect results from its ability to dampen ryanodine channel Ca2+ signaling. Funding: DAMD 17-03-1-0067 and UC TSR&TP." @default.
- W111918674 created "2016-06-24" @default.
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- W111918674 date "2008-03-01" @default.
- W111918674 modified "2023-09-24" @default.
- W111918674 title "Boric acid is a modulator of stored calcium release in DU‐145 prostate cancer cells" @default.
- W111918674 doi "https://doi.org/10.1096/fasebj.22.1_supplement.1181.16" @default.
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