<Original Ariticle>Different Ways of Cell Death Induced by HMG-CoA Reductase Inhibitor, Cerivastatin in Leukemia Cells Lines
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概要
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3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors (statins) have been shown to block tumor cell growth directly including AML cells. Here, we have studied the effect of cerivastatin, a potent statin, on the growth of AML cell lines. Growth of both HL-60 and Kasumi-1 was suppressed by cerivastatin, although the extent of suppression was much more prominent in HL-60 than in Kasumi-1. Apoptosis, induced by cerivastatin, was detected through plasma membrane alterations (by annexin V and propidium iodide (PD) and loss of mitochondrial function (by MitoTracker). In Kasumi-1 cells, both early (annexin V^+, PI^-) and late (annexin V^+, PI^+) apoptotic populations increased by cerivastatin treatment. 0n the other hand, in HL-60 cells, early apoptotic population did not appear by the addition of cerivastatin, but late apoptotic/necrotic population increased dramatically. Kasumi-1 cells, treated with cerivastatin, entered the apoptotic process by the alteration of plasma membrane, detected by annexin V staining. Then the process proceeded by depolarization of mitochondria. On the other hand, HL-60 cells, upon cerivastatin treatment, showed partial depolarization of mitochondria, then an increase of annexin V positive fractions, and finally further collapse of mitochondrial function. ln summary, we found two ways of apoptosis induction by cerivastatin treatment : one is plasma membrane alteration-preceding type (Kasumi-1), the other is mitochondria dysfunction-preceding type (HL-60).
- 愛知医科大学の論文
- 2003-06-15