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Thalidomide Suppresses the Interleukin 1β-Induced NFκB Signaling Pathway in Colon Cancer Cells

Authors
 Soo Hyun Jin  ;  Tae Il Kim  ;  Dong Soo Han  ;  Sung Kwan Shin  ;  Won Ho Kim 
Citation
 ANNALS OF THE NEW YORK ACADEMY OF SCIENCES, Vol.973 : 414-418, 2002 
Journal Title
 ANNALS OF THE NEW YORK ACADEMY OF SCIENCES 
ISSN
 0077-8923 
Issue Date
2002
MeSH
Colonic Neoplasms ; Humans ; Interleukin-1/antagonists & inhibitors ; Interleukin-1/pharmacology* ; Interleukin-8/biosynthesis ; NF-kappa B/drug effects ; NF-kappa B/metabolism* ; Signal Transduction/drug effects* ; Thalidomide/pharmacology* ; Tumor Cells, Cultured
Keywords
thalidomide ; nuclear factor κB (NFκB)
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 NFκB pathway. Thalidomide inhibited interleukin (IL) 1β-induced NFκB transcriptional activation and IL-8 production in Caco-2 colon cancer cells. In addition, thalidomide suppressed NFκB nuclear translocation, IκB degradation, and NFκB-inducing kinase (NIK)-induced NFκB transcriptional activation. These results suggest that the molecular target of the effects of thalidomide may be IκB phosphorylation by IκB kinase (IKK), whose activation follows NIK activation and precedes IκB degradation in the NFκB pathway.
Full Text
http://onlinelibrary.wiley.com/doi/10.1111/j.1749-6632.2002.tb04674.x/abstract
DOI
10.1111/j.1749-6632.2002.tb04674.x
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Internal Medicine (내과학교실) > 1. Journal Papers
Yonsei Authors
Kim, Won Ho(김원호) ORCID logo https://orcid.org/0000-0002-5682-9972
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/143514
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