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Tumor Biology |
Lurie Cancer Center, Northwestern University Medical School [X-H. Y., A. D. T.] and Departments of Medicine [X-H. Y., X. L., C. J. F.] and Pathology [B. R. B., A. D. T.], Evanston Northwestern Healthcare, Evanston, Illinois 60201, and Department of Microbiology/Immunology, Finch University of Health Sciences/The Chicago Medical School, North Chicago, Illinois 60064 [T. L. S.]
MCF-7, a breast cancer-derived cell line, is deficient of caspase 3 and relatively insensitive to many chemotherapeutic agents. To study the association of caspase 3 deficiency and chemotherapeutic resistance, we reconstituted caspase 3 in MCF-7 cells and characterized their apoptotic response to doxorubicin and etoposide. Western blots demonstrated that caspase 3 was constitutively expressed in the reconstituted MCF-7 cells. Both morphological observation and survival assays showed that caspase 3 reconstitution significantly sensitized MCF-7 cells to both drugs. Remarkably increased activation of caspases 3, 6, and 7, cleavage of cellular death substrates, and DNA fragmentation were detected in the reconstituted MCF-7 cells after drug treatment. Together, these data demonstrated a specific role for caspase 3 in chemotherapy-induced apoptosis and in activation of caspases 6 and 7. Our results also suggest that caspase 3 deficiency may contribute to chemotherapeutic resistance in breast cancer.
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