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KMID : 0603519980030010058
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Journal of Korean Association of Cancer Prevention
1998 Volume.3 No. 1 p.58 ~ p.64
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Induction of Apoptosis by Intracellular Ca2+ Inhibitors in Human Leukemic HL-60 Cells
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Lee Yong-Soo
Baek Jin-Hyen
Kim Jung-Ae
Son Han-Chul
Kwon Kyung-Sool
Kim Kyu-Won
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Abstract
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Apoptosis which plays an important role in tumorigenesis as well as embryo development has been known to be induced by the sustained rise in intracellular free Ca2+. However, many studies have shown that apoptosis is not always related with increased intracellular free calcium concentration. In the present study, the effect of several intracellular Ca2+ inhibitors on cell death was investigated in order to evaluate the role of intracellular Ca2+ signal inhibition in apoptotic cell death using HL-60 human promyelocytic leukemia cells as a model cellular system. Plasma membrane Ca2+ channel blockers (verapamil, nifedipine and diltiazem), intracellular Ca2+ release blockers (dantrolene, TMB-8 and ruthenium red), an extracellular Ca2+ chelator (EGTA) and an intracellular Ca2+ chelator (BAPT/UAM) were used as intracellular Ca2+ inhibitors in the experiments. Treatment with these agents resulted in a concentration-dependent decreased cell viability assessed by MTT assay. These agents also induced genomic DNA fragmentation, a hallmark of apoptosis, indicating that the mechanism by which these agents induce cell death was through apoptosis. No effect of cycloheximide, a protein synthesis inhibitor, on the cell death was observed, implying that new protein synthesis may not be required for the apoptosis caused by these intracellular Ca2+ inhibitors. These results suggest that the inhibition of intracellular Ca2+ signals may be involved in the induction of apoptosis in HL-60 cells.
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KEYWORD
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HL-60 cell, Apoptosis, Cycloheximide, BATA/AM, Dantrolene, Diltiazem@EGTA, Nifedipine, Ruthenium red, Verapamil
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