Inflammasome-mediated suppression of inflammation-induced colorectal cancer progression is mediated by direct regulation of epithelial cell proliferation.

Bo Hu, Eran Elinav, Richard A Flavell

Department of Immunobiology, Yale University School of Medicine, New Haven, CT, USA.

Cell cycle (Georgetown, Tex.) 2011 Jun 15

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Chronic inflammation is a risk factor for many types of human cancers, yet the precise mechanism of this strong association is largely unknown. The inflammasome is a multiprotein complex that has recently been shown to orchestrate multiple innate and adaptive immune responses, yet its potential role in inflammation-induced cancer has been little studied. We recently reported a surprising link between the inflammasome and colorectal inflammation-induced tumorigenesis. In the model, the role of caspase-1 and NLRC4 in tumorigenesis was found to be mediated by direct and profound effects on colonic epithelial cell proliferation and cell death, rather than through regulation of colonic inflammation. Herein, we discuss the recent advances and discoveries related to the role of inflammasome in inflammation-induced colorectal tumorigenesis.

Citation

Bo Hu, Eran Elinav, Richard A Flavell. Inflammasome-mediated suppression of inflammation-induced colorectal cancer progression is mediated by direct regulation of epithelial cell proliferation. Cell cycle (Georgetown, Tex.). 2011 Jun 15;10(12):1936-9