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Blood, Vol. 93 No. 7 (April 1), 1999:
pp. 2386-2394
Sodium Salicylate Activates Caspases and Induces Apoptosis of Myeloid
Leukemia Cell Lines
Lidija Klampfer,
Jörg Cammenga,
Hans-Georg Wisniewski, and
Stephen D. Nimer
From the Laboratory of Molecular Aspects of Hematopoiesis and
Department of Medicine, Memorial Sloan-Kettering Cancer Center, New
York; and New York University Medical Center, Department of
Microbiology, New York, NY.
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-XL 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.
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