TY - JOUR
T1 - Inflammasomes and intestinal tumorigenesis
AU - Zaki, Md Hasan
AU - Lamkanfi, Mohamed
AU - Kanneganti, Thirumala Devi
N1 - Funding Information:
We acknowledge researchers who have contributed to this field, whose work was not cited or was cited through review articles because of space limitations. This work was supported by National Institute of Health Grants ( R01AR056296 and AI088177 ), and the American Lebanese Syrian Associated Charities (ALSAC) to T-D.K. M.L. is supported by the European Union Framework Program 7 Marie-Curie grant 256432 and the Fund for Scientific Research-Flanders. M.H.Z. is supported by Gephardt fellowship.
PY - 2011
Y1 - 2011
N2 - Colorectal cancer is a major health problem in developed countries. Chronic intestinal inflammation predisposes individuals to the development of colorectal cancer. The intracellular NOD-like receptors (NLRs) have emerged as crucial regulators of intestinal inflammation and colorectal tumorigenesis. Activation of several NLRs leads to the formation of a protein complex called the inflammasome, which then triggers the activation of the cysteine protease caspase-1 and the downstream maturation and secretion of the inflammatory cytokines interleukin (IL)-1β and -18. Defective inflammasome signaling in the gut contributes to colitis and colorectal tumorigenesis by increasing the permeability of the epithelial barrier, dysregulating the proliferation of epithelial cells, and inducing oncogenic mediators. In this review, we discuss our current knowledge on how the inflammasome protects against colorectal tumorigenesis.
AB - Colorectal cancer is a major health problem in developed countries. Chronic intestinal inflammation predisposes individuals to the development of colorectal cancer. The intracellular NOD-like receptors (NLRs) have emerged as crucial regulators of intestinal inflammation and colorectal tumorigenesis. Activation of several NLRs leads to the formation of a protein complex called the inflammasome, which then triggers the activation of the cysteine protease caspase-1 and the downstream maturation and secretion of the inflammatory cytokines interleukin (IL)-1β and -18. Defective inflammasome signaling in the gut contributes to colitis and colorectal tumorigenesis by increasing the permeability of the epithelial barrier, dysregulating the proliferation of epithelial cells, and inducing oncogenic mediators. In this review, we discuss our current knowledge on how the inflammasome protects against colorectal tumorigenesis.
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U2 - 10.1016/j.ddmec.2011.11.003
DO - 10.1016/j.ddmec.2011.11.003
M3 - Review article
C2 - 22768019
AN - SCOPUS:84860339104
SN - 1740-6765
VL - 8
SP - e71-e78
JO - Drug Discovery Today: Disease Mechanisms
JF - Drug Discovery Today: Disease Mechanisms
IS - 3-4
ER -