Mechanism of estrogens-induced increases in intracellular Ca2+ in PC3 human prostate cancer cells

Jong Khing Huang*, Chung Ren Jan

*Corresponding author for this work

Research output: Contribution to journalJournal Article peer-review

29 Scopus citations

Abstract

BACKGROUND. The effect of estrogens (diethylstilbestrol [DES], 17β-estradiol) on intracellular Ca2+ concentrations ([Ca2+]i) in hormone-insensitive PC3 human prostate cancer cells was examined. METHODS. [Ca2+]i changes in suspended cells were measured by using the Ca2+-sensitive fluorescent dye fura-2. RESULTS. Estrogens (1-20 μM) increased [Ca2+]i concentration-dependently with DES being more potent. Ca2+ removal inhibited 50 ± 10% of the signal. In Ca2+-free medium, pretreatment with 20 μM estrogens abolished the [Ca2+]i increases induced by 2 μM carbonylcyanide m-chlorophenylhydrazone (CCCP, a mitochondrial uncoupler) and 1 μM thapsigargin (an endoplasmic reticulum Ca2+ pump inhibitor), but pretreatment with CCCP and thapsigargin did not alter DES-induced Ca2+ release and partly inhibited 17β-estradiol-induced Ca2+ release. Addition of 3 mM Ca2+ increased [Ca2+]i in cells pretreated with 1-20 μM estrogens in Ca2+-free medium. Pretreatment with 1 μM U73122 to block phospholipase C-coupled inositol 1,4,5-trisphosphate formation did not alter estrogens-induced Ca2+ release. The effect of 20 μM estrogen on [Ca2+]i was not affected by pretreatment with 0.1 μM estrogens. CONCLUSIONS. Estrogen induced significant Ca2+ release and Ca2+ influx in an inositol 1,4,5-trisphosphate-independent manner in PC3 cells. These effects of estrogens on Ca2+ signaling appear to be nongenomic.

Original languageEnglish
Pages (from-to)141-148
Number of pages8
JournalProstate
Volume47
Issue number3
DOIs
StatePublished - 15 05 2001
Externally publishedYes

Keywords

  • 17β-estradiol
  • Ca
  • Diethylstilbestrol
  • PC3
  • Prostate cancer cells

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