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• W1968240982 endingPage "224" @default.
• W1968240982 startingPage "219" @default.
• W1968240982 abstract "Cancer cells are characterized by a high rate of glycolysis, which is their primary energy source. We show here that a rise in intracellular-free calcium ion (Ca2+), induced by Ca2+-ionophore A23187, exerted a deleterious effect on glycolysis and viability of B16 melanoma cells. Ca2+-ionophore caused a dose-dependent detachment of phosphofructokinase (EC 2.7.1.11), one of the key enzymes of glycolysis, from cytoskeleton. It also induced a decrease in the levels of glucose 1,6-bisphosphate and fructose 1,6-bisphosphate, the two stimulatory signal molecules of glycolysis. All these changes occurred at lower concentrations of the drug than those required to induce a reduction in viability of melanoma cells. We also found that low concentrations of Ca2+-ionophore induced an increase in adenosine 5′-triphosphate (ATP), which most probably resulted from the increase in mitochondrial-bound hexokinase, which reflects a defence mechanism. This mechanism can no longer operate at high concentrations of the Ca2+-ionophore, which causes a decrease in mitochondrial and cytosolic hexokinase, leading to a drastic fall in ATP and melanoma cell death. The present results suggest that drugs which are capable of inducing accumulation of intracellular-free Ca2+ in melanoma cells would cause a reduction in energy-producing systems, leading to melanoma cell death." @default.
• W1968240982 created "2016-06-24" @default.
• W1968240982 creator A5025037399 @default.
• W1968240982 creator A5025413631 @default.
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• W1968240982 date "1999-08-27" @default.
• W1968240982 modified "2023-10-14" @default.
• W1968240982 title "Ca2+-induced changes in energy metabolism and viability of melanoma cells" @default.
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• W1968240982 doi "https://doi.org/10.1038/sj.bjc.6690680" @default.
• W1968240982 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2362860" @default.
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