PMID:
Chin J Physiol. 2017 Oct 31 ;60(5):275-283. PMID: 28950692
Abstract Title:
Effect of Carvacrol on Ca²⁺ Movement and Viability in PC3 Human Prostate Cancer Cells.
Abstract:
Carvacrol, a monoterpenic phenol compound, has been shown to possess various biological
effects in different models. However, the effect of carvacrol on intracellular Ca²⁺ and its related
physiology in human prostate cancer is unknown. This study explored the effect of carvacrol on
cytosolic free Ca²⁺ levels ([Ca²⁺]i) and viability in PC3 human prostate cancer cells. Fura-2, a Ca²⁺-
sensitive fluorescent dye, was used to assess [Ca²⁺]i. Cell viability was measured by the detecting
reagent WST-1. Carvacrol at concentrations of 200-800 μM caused [Ca²⁺]i rises in a concentration-dependent
manner. Removal of extracellular Ca²⁺ reduced carvacrol’s effect by approximately 60%.
Carvacrol-induced Ca²⁺ entry was confirmed by Mn²⁺ entry-induced quench of fura-2 fluorescence,
and was inhibited by approximately 30% by nifedipine, econazole, SKF96365, and the protein kinase
C (PKC) inhibitor GF109203X. In Ca²⁺-free medium, treatment with the endoplasmic reticulum Ca²⁺
pump inhibitor thapsigargin (TG) abolished carvacrol-induced [Ca²⁺]i rises. Treatment with
carvacrol also abolished TG-induced [Ca²⁺]i rises. Carvacrol-induced Ca²⁺ release from the
endoplasmic reticulum was abolished by inhibition of phospholipase C (PLC). Carvacrol killed cells
at concentrations of 200-600 μM in a concentration-dependent fashion. Chelating cytosolic Ca²⁺ with
BAPTA/AM did not prevent carvacrol’s cytotoxicity. Together, in PC3 cells, carvacrol 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. Carvacrol also induced
Ca²⁺-dissociated cell death.
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