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Deficiency of Caspase-3 in MCF7 Cells Blocks Bax-mediated Nuclear Fragmentation but not Cell Death¹

Departments of Thoracic and Cardiovascular Surgery [S. K., J. G., S. G. S., J. A. R., B. F.] and Molecular Pathology [T. J. M.], The University of Texas M. D. Anderson Cancer Center, Houston, Texas 77030, and Department of Obstetrics and Gynecology, Yamanashi Medical University, Yamanashi 409-3898, Japan [T. H.]

Caspase-3 plays a critical role in a proteolytic cascade within the apoptosis signal pathway; this enzyme is commonly activated by numerous death signals and cleaves a variety of important cellular proteins. Using caspase-3-deficient MCF7 cells and clones stably transfected with the caspase-3 gene (MCF7/Casp3), we evaluated the role of caspase-3 in Bax-induced apoptosis. Bax overexpression induced cell death in both parental MCF7 cells and MCF7/Casp3 cells. The introduction of the caspase-3 gene did not change the rate of cell death. Caspase-3-deficient parental MCF7 cells, however, failed to undergo morphological nuclear and DNA fragmentation, whereas MCF7/casp3 cells displayed intact nuclear dismantling and DNA fragmentation. Caspase-3 deficiency, however, did not affect Bax-induced levels of poly(ADP-ribose) polymerase cleavage, caspase-6 activation, and lamin B cleavage. Together, these results suggest that a deficit in caspase-3 is not sufficient to block Bax-induced cell death.

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