Sodium salicylate activates caspases and induces apoptosis of myeloid leukemia cell lines

被引:128
作者
Klampfer, L
Cammenga, J
Wisniewski, HG
Nimer, SD
机构
[1] Mem Sloan Kettering Canc Ctr, Dept Med, New York, NY 10021 USA
[2] Mem Sloan Kettering Canc Ctr, Lab Mol Aspects Hematopoiesis, New York, NY 10021 USA
[3] NYU, Dept Microbiol, Med Ctr, New York, NY 10016 USA
关键词
D O I
10.1182/blood.V93.7.2386.407k15_2386_2394
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Nonsteroidal antiinflammatory agents (NSAIA) have been shown to exert potent chemopreventive activity against colon, lung, and breast cancers. In this study, we show that at pharmacological concentrations (1 to 3 mmol/L) sodium salicylate (Na-Sal) can potently induce programmed cell death in several human myeloid leukemia cell lines, including TF-1, U937, CMK-1, HL-60, and Mo7e. TF-1 cells undergo rapid apoptosis on treatment with Na-Sal, as indicated by increased annexin V binding capacity, cpp-32 (caspase-3) activation, and cleavage of poly (ADP-ribose) polymerase (PARP) and gelsolin. In addition, the expression of MCL-1, an antiapoptotic member of the BCL-2 family, is downregulated during Na-Sal-induced cell death, whereas the expression of BCL-2, BAX, and BCL-X-L is unchanged. Z-VAD, a potent caspase inhibitor, prevents the cleavage of PARP and gelsolin and rescues cells from Na-Sal-induced apoptosis. In addition, we show that Na-Sal accelerates growth factor withdrawal-induced apoptosis and synergizes with daunorubicin to induce apoptosis in TF-1 cells. Thus, our data provide a potential mechanism for the chemopreventive activity of NSAIA and suggest that salicylates may have therapeutic potential for the treatment of human leukemia. (C) 1999 by The American Society of Hematology.
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页码:2386 / 2394
页数:9
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