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- Ahead-of-Print
Effect of Thymol on Ca^(2+) Homeostasis and Viability in PC3 Human Prostate Cancer Cells
摘要
Thymol is a phenolic compound that affects physiology in different cell models. However, whether thymol affects Ca^(2+) homeostasis in prostate cancer cells is unknown. The action of this compound on cytosolic Ca^(2+) concentrations ([Ca^(2+)]_i) and viability in PC3 human prostate cancer cells was explored. The results show that thymol at concentrations of 100-1500 μM caused [Ca^(2+)]_i rises in a concentration-dependent manner. Removal of extracellular Ca^(2+) reduced thymol's effect by approximately 80%. Thymol-induced Ca^(2+) entry was confirmed by Mn^(2+) entry-induced quench of fura-2 fluorescence, and was inhibited by approximately 30% by Ca^(2+) entry modulators (nifedipine, econazole, SKF96365), and the protein kinase C (PKC) inhibitor GF109203X. In Ca^(2+)-free medium, treatment with the endoplasmic reticulum Ca^(2+) pump inhibitor thapsigargin abolished thymol-induced [Ca^(2+)]_i rises. Treatment with thymol also abolished thapsigargin-induced [Ca^(2+)]_i rises. Thymol-induced Ca^(2+) release from the endoplasmic reticulum was abolished by the phospholipase C (PLC) inhibitor U73122. Thymol at 100-900 μM decreased cell viability, which was not reversed by pretreatment with the Ca^(2+) chelator 1,2-bis(2-aminophenoxy) ethane-N,N,N',N'-tetraacetic acid-acetoxymethyl ester (BAPTA/AM). Together, in PC3 cells, thymol induced [Ca^(2+)]_i rises by inducing PLC-dependent Ca^(2+) release from the endoplasmic reticulum and Ca^(2+) entry via PKC-sensitive store-operated Ca^(2+) channels and other unknown channels. Thymol also induced Ca^(2+)-dissociated cell death.
參考文獻
延伸閱讀
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