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[Cancer Research 63, 290-295, January 15, 2003]
© 2003 American Association for Cancer Research

Advances in Brief

Apoptosis Caused by Chemotherapeutic Inhibition of Nuclear Factor-{kappa}B Activation1

Debajit K. Biswas2, Katherine J. Martin, Cliona McAlister, Antonio P. Cruz, Edgard Graner, Sun-chun Dai and Arthur B. Pardee

Dana-Farber Cancer Institute, Department of Cancer Biology, Boston, Massachusetts 02115

Both the protein kinase C ({alpha}/ß) inhibitor Go6976 and expression of dominant-negative nuclear factor (NF)-{kappa}B inhibitor kinase mutants: (a) blocked the growth and caused regression of a mammary tumor insyngeneic mice; (b) inhibited epidermal growth factor (EGF)-induced activation, nuclear translocation, and DNA-binding activity of NF-{kappa}B; and (c) caused apoptosis of EGF-stimulated cultured mammary tumor cells. cDNA microarray analysis revealed that these treatments reversed the expression changes of a subset of genes altered by EGF treatment. These included: up-regulation of proapoptotic genes of the tumor necrosis factor (TNF) pathway, death-associated protein (DAP) kinase, p53, and p21/Waf1; and down-regulation of inhibitors of apoptosis: inhibitor of apoptosis(IAP)-1 and X-IAP, TNF receptor-associated factor (TRAF)-2, and factors OX40 and 4-1BB. These results and our previous studies suggest the practicality of a target-directed chemotherapy for EGF-responsive breast cancers, by blocking NF-{kappa}B activation and thereby reinstating apoptosis.




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