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NO-donating aspirin inhibits the growth of leukemic Jurkat cells and modulates beta-catenin expression.

Nath N, Labaze G, Rigas B, Kashfi K

Department of Physiology and Pharmacology, City University of New York Medical School, New York, NY 10031, USA.

beta-Catenin has been implicated in leukemic cell proliferation. We compared the effects of aspirin (ASA) and the ortho, meta, and para positional isomers of NO-donating aspirin (NO-ASA) on cell growth and beta-catenin expression in human Jurkat T leukemic cells. Cell growth inhibition was strong: IC(50) for p-, o-, and m- were 20+/-1.6 (mean+/-SEM), 15+/-1.5, and 200+/-12 microM, respectively, in contrast to that of ASA (3200+/-375 microM). The para isomer of NO-ASA degraded beta-catenin in a dose- and time-dependent manner coinciding with increasing expression of activated caspase-3. The caspase inhibitor ZVAD blocked beta-catenin cleavage by p-NO-ASA and partially reversed cell growth inhibition by p-NO-ASA but not that by ASA. A denitrated analog of p-NO-ASA did not degrade beta-catenin indicating the importance of the NO-donating moiety. Our findings suggest that NO-ASA merits further study as an agent against leukemia.

Published 29 November 2004 in Biochem Biophys Res Commun, 326(1): 93-9.
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