Mechanism of estrogens‐induced increases in intracellular Ca<sup>2+</sup> in PC3 human prostate cancer cells

Huang, Jong‐Khing; Jan, Chung‐Ren

doi:10.1002/pros.1057

Cited by 29 publications

(22 citation statements)

References 25 publications

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“…This conclusion is consistent with results from several suspended cell preparations including MG63 human osteosarcoma cells [10], PC3 human prostate cancer cells [21], renal tubular cells [22], and human breast cancer cells [9]. In each of these cases, DES in micromolar concentrations continued to increase [Ca 2+ ] i after the removal of [Ca 2+ ] o , thus indicating that the drug released Ca 2+ from intracellular stores without requiring an inwards electrochemical gradient.…”

Section: Discussionsupporting

confidence: 90%

Diethylstilbestrol increases intracellular calcium in lens epithelial cells

Samadi¹,

Cenedella²,

Carlson

2005

Pflugers Arch - Eur J Physiol

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The effects of diethylstilbestrol (DES) on steady-state intracellular calcium concentration ([Ca(2+)](i)) and resting Ca(2+) influx were examined in primary cultures of bovine lens epithelial cells using conventional fluorometric techniques (Fura-2). At low concentrations (10 microM), DES usually induced relatively rapid increases in [Ca(2+)](i) that occurred over an interval of 10-50 s and that persisted for several minutes in the continued presence of the drug. In about 10% of the cells, cyclic oscillations in [Ca(2+)](i) were seen after adding 10 microM DES. At higher concentrations (100 microM), the drug induced more prolonged increases in [Ca(2+)](i) lasting several minutes. DES did not affect Mn(2+) quench determinations of resting Ca(2+) influx, and neither 100 microM GdCl(3), which blocked resting Ca(2+) influx, nor low [Ca(2+)](o) solutions substantially diminished the influence of DES on [Ca(2+)](i). Pretreatment of cells with the smooth endoplasmic reticulum Ca(2+) ATPase (SERCA) inhibitors cyclopiazonic acid (CPA) or thapsigargin completely abolished the effect of 10 microM DES on [Ca(2+)](i), while the IP(3) receptor blocker 2-aminoethoxydiphenyl borane (2-APB) had no effect. These results indicate that DES releases CPA-sensitive stores of intracellular Ca(2+), perhaps by inhibiting SERCA-dependent Ca(2+) sequestration.

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Section: Discussionsupporting

confidence: 90%

Diethylstilbestrol increases intracellular calcium in lens epithelial cells

Samadi¹,

Cenedella²,

Carlson

2005

Pflugers Arch - Eur J Physiol

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“…In PC3 cells, the endoplasmic reticulum has been shown to be a major Ca 2+ store Huang and Jan, 2001;Jiann et al, 2002;Jan et al, 2002). Consistently, NDGA appears to solely release Ca 2+ from thapsigargin-sensitive endoplasmic reticulum Ca 2+ stores, based on the results that depletion of the stores with thapsigargin abolished NDGA-induced Ca 2+ release.…”

Section: Discussionmentioning

confidence: 64%

Nordihydroguaiaretic acid-induced Ca2+ handling and cytotoxicity in human prostate cancer cells

et al. 2004

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“…Rapid effects of estrogens occur in multiple areas of the nervous system [e.g., hypothalamus (Qiu et al, 2003), hippocampus (Gu et al, 1999), and neostriatum (Mermelstein et al, 1996)], in various peripheral tissues [e.g., adipocytes (Dos Santos et al, 2002) and gametes (Morley et al, 1992;Luconi et al, 2001)], and in tumors (Aronica et al, 1994;Huang and Jan, 2001). Previously, studies of these effects were based on the application of exogenous E2 and did not provide information regarding the origin of estrogens that induce rapid effects in vivo.…”

Section: Expression Of Aromatase In the Spinal Cord Of Other Speciesmentioning

confidence: 99%

Rapid Regulation of Pain by Estrogens Synthesized in Spinal Dorsal Horn Neurons

2004

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In addition to exerting genomic actions via nuclear receptors within hours to days, estrogens also regulate neuronal activity much faster (within seconds) by activating neuronal membrane receptors coupled to intracellular second-messenger pathways. To date, the origin of estrogens inducing rapid effects in the brain remains unclear, although it is often ascribed to the gonads. We report here that an acute blockade of the endogenous synthesis of estrogens in the quail spinal dorsal horn markedly reduced, within 1 min, the behavioral responsiveness to a thermal painful stimulus. Similar rapid effects in the opposite direction were induced by estradiol. This finding identifies a new paracrine and nongenomic mechanism for the regulation of pain by estrogens. Such regulation was assumed previously to result only from slow genomic actions of estrogens arising from the ovaries. Also, quite importantly, this finding suggests that the numerous rapid nongenomic effects of estrogens in the CNS could depend on their immediate local production by the enzyme aromatase, independently from the gonads.

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

Abstract: Estrogen induced significant Ca(2+) release and Ca(2+) influx in an inositol 1,4,5-trisphosphate-independent manner in PC3 cells. These effects of estrogens on Ca(2+) signaling appear to be nongenomic. Prostate 47:141-148, 2001.

Cited by 29 publications

References 25 publications

Diethylstilbestrol increases intracellular calcium in lens epithelial cells

Diethylstilbestrol increases intracellular calcium in lens epithelial cells

Nordihydroguaiaretic acid-induced Ca2+ handling and cytotoxicity in human prostate cancer cells

Rapid Regulation of Pain by Estrogens Synthesized in Spinal Dorsal Horn Neurons

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

Abstract: Estrogen induced significant Ca(2+) release and Ca(2+) influx in an inositol 1,4,5-trisphosphate-independent manner in PC3 cells. These effects of estrogens on Ca(2+) signaling appear to be nongenomic. Prostate 47:141-148, 2001.

Cited by 29 publications

References 25 publications

Diethylstilbestrol increases intracellular calcium in lens epithelial cells

Diethylstilbestrol increases intracellular calcium in lens epithelial cells

Nordihydroguaiaretic acid-induced Ca2+ handling and cytotoxicity in human prostate cancer cells

Rapid Regulation of Pain by Estrogens Synthesized in Spinal Dorsal Horn Neurons

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Product

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