Effect of thapsigargin on Ca2+fluxes and viability in human prostate cancer cells
| Autor: | Wei-Chuan Liao, I-Shu Chen, Yi-Chau Lu, Jue-Long Wang, Chung-Ren Jan, Chin-Man Ho, Jong-Khing Huang, Hong-Tai Chang, Su-Shung Shu, Chiang-Ting Chou, Jeng-Yu Tsai, Shuih-Inn Liu, Ko-Long Lin, Chun-Chi Kuo |
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| Rok vydání: | 2011 |
| Předmět: |
medicine.medical_specialty
Thapsigargin biology Fura-2 Endoplasmic reticulum Cell Biology Biochemistry Molecular biology chemistry.chemical_compound Phospholipase A2 Endocrinology chemistry Internal medicine Cancer cell medicine biology.protein Extracellular Molecular Biology Protein kinase C Carcinogen |
| Zdroj: | Journal of Receptors and Signal Transduction. 31:247-255 |
| ISSN: | 1532-4281 1079-9893 |
| DOI: | 10.3109/10799893.2011.563311 |
| Popis: | Effect of the carcinogen thapsigargin on human prostate cancer cells is unclear. This study examined if thapsigargin altered basal [Ca2+]i levels in suspended PC3 human prostate cancer cells by using fura-2 as a Ca2+-sensitive fluorescent probe. Thapsigargin at concentrations between 10 nM and 10 µM increased [Ca2+]i in a concentration-dependent fashion. The Ca2+ signal was reduced partly by removing extracellular Ca2+ indicating that Ca2+ entry and release both contributed to the [Ca2+]i rise. This Ca2+ influx was inhibited by suppression of phospholipase A2, but not by inhibition of store-operated Ca2+ channels or by modulation of protein kinase C activity. In Ca2+-free medium, pretreatment with the endoplasmic reticulum Ca2+ pump inhibitor 2,5-di-(t-butyl)-1,4-hydroquinone (BHQ) nearly abolished thapsigargin-induced Ca2+ release. Conversely, pretreatment with thapsigargin greatly reduced BHQ-induced [Ca2+]i rise, suggesting that thapsigargin released Ca2+ from the endoplasmic reticulum. Inhibition of p... |
| Databáze: | OpenAIRE |
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