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[Cancer Research 62, 18-23, January 1, 2002]
© 2002 American Association for Cancer Research

Advances in Brief

Smac Is Required for Cytochrome c-induced Apoptosis in Prostate Cancer LNCaP Cells1

Jonathan P. Carson2, Marcelina Behnam2, Jennifer N. Sutton, Chunying Du, Xiaodong Wang, Donald F. Hunt, Michael J. Weber and George Kulik3

Departments of Microbiology [J. P. C., M. B., M. J. W., G. K.] and Chemistry [J. N. S., D. F. H.] at the University of Virginia, Charlottesville, Virginia 22908, and Howard Hughes Medical Institute, Department of Biochemistry, University of Texas Southwestern Medical Center, Dallas, Texas 75235 [C. D., X. W.]

Release of cytochrome c from mitochondria to cytosol has been identified as one of the central events of apoptosis. Direct injection of cytochrome c induces apoptosis in some but not in all cell types. We observed that LNCaP prostate cancer cells failed to undergo apoptosis induced by cytochrome c microinjections. Microinjection of cytochrome c with another mitochondrial protein, Smac, was sufficient to activate caspases, however. Smac is believed to function as a neutralizer of caspase inhibitors, and mass spectrometry analysis identified XIAP as a predominant Smac binding protein in LNCaP cells. These findings are consistent with a requirement for a release of Smac from mitochondria to enable caspase activation in prostate cells. Indeed, translocation of Smac from mitochondria to cytosol was observed in LNCaP cells that undergo apoptosis and was inhibited by epidermal growth factor, which is a survival factor for these cells. These results further emphasize the central role of mitochondria in the regulation of apoptosis in prostate cancer cells.




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