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[Cancer Research 60, 3838-3847, July 15, 2000]
© 2000 American Association for Cancer Research

Immunology

Oleandrin Suppresses Activation of Nuclear Transcription Factor-{kappa}B, Activator Protein-1, and c-Jun NH2-Terminal Kinase1

Sunil K. Manna, Nand K. Sah2, Robert A. Newman, Angela Cisneros and Bharat B. Aggarwal3

Cytokine Research Laboratory, Department of Bioimmunotherapy [S. K. M., N. K. S., B. B. A.], and Pharmaceutical Development Center [R. A. N., A. C.], The University of Texas M. D. Anderson Cancer Center, Houston, Texas 77030

Agents that can suppress the activation of nuclear factor-{kappa}B (NF-{kappa}B) and activator protein-1 (AP-1) may be able to block tumorigenesis and inflammation. Oleandrin, a polyphenolic cardiac glycoside derived from the leaves of Nerium oleander, is a candidate NF-{kappa}B and AP-1 modulator. We investigated the effect of oleandrin on NF-{kappa}B activation induced by inflammatory agents. Oleandrin blocked tumor necrosis factor (TNF)-induced activation of NF-{kappa}B in a concentration- and time-dependent manner. This effect was mediated through inhibition of phosphorylation and degradation of I{kappa}B{alpha}, an inhibitor of NF-{kappa}B. A proprietary hot water extract of oleander (Anvirzel) also blocked TNF-induced NF-{kappa}B activation; subsequent fractionation of the extract revealed that this activity was attributable to oleandrin. The effects of oleandrin were not cell type specific, because it blocked TNF-induced NF-{kappa}B activation in a variety of cells. NF-{kappa}B-dependent reporter gene transcription activated by TNF was also suppressed by oleandrin. The TNF-induced NF-{kappa}B activation cascade involving TNF receptor 1/TNF receptor-associated death domain/TNF receptor-associated factor 2/NF-{kappa}B-inducing kinase/I{kappa}B{alpha} kinase was interrupted at the TNF receptor-associated factor 2 and NF-{kappa}B-inducing kinase sites by oleandrin, thus suppressing NF-{kappa}B reporter gene expression. Oleandrin blocked NF-{kappa}B activation induced by phorbol ester and lipopolysaccharide. Oleandrin also blocked AP-1 activation induced by TNF and other agents and inhibited the TNF-induced activation of c-Jun NH2-terminal kinase. Overall, our results indicate that oleandrin inhibits activation of NF-{kappa}B and AP-1 and their associated kinases. This may provide a molecular basis for the ability of oleandrin to suppress inflammation and perhaps tumorigenesis.




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Cancer Research Clinical Cancer Research
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Molecular Cancer Research Cancer Prevention Research
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Copyright © 2000 by the American Association for Cancer Research.