Abstract Title:

Effect of thymol on Ca²⁺ homeostasis and viability in PC3 human prostate cancer cells.

Abstract Source:

Chin J Physiol. 2017 02 28 ;60(1):32-40. PMID: 28052644

Abstract Author(s):

Jeng-Hsien Yeh, Chiang-Ting Chou, I-Shu Chen, Ti Lu, Ko-Long Lin, Chia-Cheng Yu, Wei-Zhe Liang, Hong-Tai Chang, Chun-Chi Kuo, Chin-Man Ho, Wen-Teng Chang, Pochuen Shieh, Chung-Ren Jan

Article Affiliation:

Jeng-Hsien Yeh


Thymol is a phenolic compound that affects physiology in different cell models. However, whether thymol affects Ca²⁺ homeostasis in prostate cancer cells is unknown. The action of this compound on cytosolic Ca²⁺ concentrations ([Ca²⁺]i) and viability in PC3 human prostate cancer cells was explored. The results show that thymol at concentrations of 100-1500 μM caused [Ca²⁺]i rises in a concentration-dependent manner. Removal of extracellular Ca²⁺ reduced thymol’s effect by approximately 80%. Thymol-induced Ca²⁺ entry was confirmed by Mn²⁺ entry-induced quench of fura-2 fluorescence, and was inhibited by approximately 30% by Ca²⁺ entry modulators (nifedipine, econazole, SKF96365),and the protein kinase C (PKC) inhibitor GF109203X. In Ca²⁺-free medium, treatment with the endoplasmic reticulum Ca²⁺ pump inhibitor thapsigargin abolished thymol-induced [Ca²⁺]i rises. Treatment with thymol also abolished thapsigargin-induced [Ca²⁺]i rises. Thymol-induced Ca²⁺ 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 Ca²⁺ chelator 1,2-bis(2-aminophenoxy) ethane-N,N,N’,N’-tetraacetic acid-acetoxymethyl ester (BAPTA/AM). Together, in PC3 cells, thymol induced [Ca²⁺]i rises by inducing PLC-dependent Ca²⁺ release from the endoplasmic reticulum and Ca²⁺ entry via PKC-sensitive store-operated Ca²⁺ channels and other unknown channels. Thymol also induced Ca²⁺-dissociated cell death.

Study Type : In Vitro Study
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Pharmacological Actions : Cytotoxicity

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