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Papers In Press, published online ahead of print May 16, 2001
J. Biol. Chem, 10.1074/jbc.C100074200
Submitted on February 6, 2001
Revised on May 11, 2001
Accepted on May 16, 2001
Adult Oncology, Dana-Farber Cancer Institute, Mayer 557, Boston, MA 02115
Corresponding Author: kenneth_anderson{at}dfci.harvard.edu
Smac, a second mitochondria-derived activator of caspases, promotes caspase activation in the cytochrome-c (cyto-c)/Apaf-1/ caspase-9 pathway. Here, we show that treatment of multiple myeloma (MM) cells with Dexamethasone (Dex) triggers the release of Smac from mitochondria to cytosol and activates caspase-9 without concurrent release of cyto-c and Apaf-1 oligomerization. Smac binds to XIAP (an inhibitor of apoptosis protein) and thereby, eliminates its inhibitory effect on caspase-9. Interleukin-6 (IL-6), a growth factor for MM, blocks Dex-induced apoptosis and prevents release of Smac. Taken together, these findings demonstrate that Smac plays a functional role in mediating Dex-induced caspase-9 activation and apoptosis in MM cells.
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