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Ann N Y Acad Sci. 2002 Nov;973:414-8.

Thalidomide suppresses the interleukin 1beta-induced NFkappaB signaling pathway in colon cancer cells.

Author information

1
Department of Internal Medicine and Institute of Gastroenterology, Brain Korea 21 Project for Medical Science, Yonsei University College of Medicine, Seoul, Korea.

Abstract

Thalidomide has been shown to have both antiinflammatory and antiangiogenic effects in several diseases. However, its cellular target and mechanism of action are poorly understood. We investigated the action mechanism of thalidomide through the NFkappaB pathway. Thalidomide inhibited interleukin (IL) 1beta-induced NFkappaB transcriptional activation and IL-8 production in Caco-2 colon cancer cells. In addition, thalidomide suppressed NFkappaB nuclear translocation, IkappaB degradation, and NFkappaB-inducing kinase (NIK)-induced NFkappaB transcriptional activation. These results suggest that the molecular target of the effects of thalidomide may be IkappaB phosphorylation by IkappaB kinase (IKK), whose activation follows NIK activation and precedes IkappaB degradation in the NFkappaB pathway.

[Indexed for MEDLINE]

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