| Inflammasome-mediated suppression of inflammation-induced colorectal cancer progression is mediated by direct regulation of epithelial cell proliferation. | |
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MedLine Citation:
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PMID: 21555913 Owner: NLM Status: Publisher |
Abstract/OtherAbstract:
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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 multi-protein complex which 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 report 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. |
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Authors:
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Bo Hu; Erah Elinav; Richard A Flavell |
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Publication Detail:
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Type: JOURNAL ARTICLE Date: 2011-6-15 |
Journal Detail:
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Title: Cell cycle (Georgetown, Tex.) Volume: 10 ISSN: 1551-4005 ISO Abbreviation: - Publication Date: 2011 Jun |
Date Detail:
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Created Date: 2011-5-10 Completed Date: - Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 101137841 Medline TA: Cell Cycle Country: - |
Other Details:
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Languages: ENG Pagination: - Citation Subset: - |
Affiliation:
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Yale University School of Medicine; New Haven, CT USA. |
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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