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Biochemistry and Biophysics |
Department of Pharmaceutics and Pharmacodynamics, Center for Pharmaceutical Biotechnology, College of Pharmacy, University of Illinois at Chicago, Chicago, Illinois 60612 [R. Y., S. M., A-N. T. K.], and Human Genome Sciences, Rockville, Maryland 20850 [S. R., J. N.]
Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) has been
reported to induce cell death in a variety of transformed cells but
spared the normal cells. In this study, we examined its potential
against advanced prostate cancer cells. Treatment of PC-3 and DU145
cells with TRAIL caused a rapid apoptotic cell death, whereas tumor
necrosis factor-
(TNF-) is ineffective unless in the presence of
the protein synthesis inhibitor cycloheximide. The induction of
apoptosis by TRAIL in PC-3 cells was mediated by a death receptor, DR
4, and the downstream caspases. Treatment of PC-3 cells with TRAIL also
activated c-Jun NH2-terminal kinase 1 (JNK1); however,
inhibition of JNK1 activation by its dominant-negative mutant had
little effect on TRAIL-induced apoptosis. Furthermore, TRAIL weakly
stimulated nuclear factor 
B activity in PC-3 cells. Interestingly,
activation of nuclear factor B pathway by pretreatment with TNF-
did not prevent the induction of apoptosis by TRAIL. These data
indicate that TRAIL triggers apoptosis in advanced prostate cancer
cells through the activation of caspase cascades, which appears to be
independent of TNF-- and JNK-mediated mechanisms.
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