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http://purl.uniprot.org/citations/23696660http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/23696660http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/23696660http://www.w3.org/2000/01/rdf-schema#comment"The microbiota is pivotal in the pathogenesis of inflammatory bowel disease (IBD)-associated inflammation-induced colorectal cancer (CRC), yet mechanisms for these effects remain poorly characterized. Here, we demonstrate that aberrant inflammasome-induced microbiota plays a critical role in CRC development, where mice deficient in the NOD-like receptor family pyrin domain containing 6 (NLRP6) inflammasome feature enhanced inflammation-induced CRC formation. Intriguingly, WT mice cohoused either with inflammasome-deficient mice or with mice lacking IL-18 feature exacerbated inflammation-induced CRC compared with singly housed WT mice. Enhanced tumorigenesis is dependent on microbiota-induced chemokine (C-C motif) ligand 5 (CCL5)-driven inflammation, which in turn promotes epithelial cell proliferation through local activation of the IL-6 pathway, leading to cancer formation. Altogether, our results mechanistically link the altered microbiota with the pathogenesis of inflammation-induced CRC and suggest that in some conditions, microbiota components may transfer CRC susceptibility between individuals."xsd:string
http://purl.uniprot.org/citations/23696660http://purl.org/dc/terms/identifier"doi:10.1073/pnas.1307575110"xsd:string
http://purl.uniprot.org/citations/23696660http://purl.org/dc/terms/identifier"doi:10.1073/pnas.1307575110"xsd:string
http://purl.uniprot.org/citations/23696660http://purl.uniprot.org/core/author"Hu B."xsd:string
http://purl.uniprot.org/citations/23696660http://purl.uniprot.org/core/author"Hu B."xsd:string
http://purl.uniprot.org/citations/23696660http://purl.uniprot.org/core/author"Hao L."xsd:string
http://purl.uniprot.org/citations/23696660http://purl.uniprot.org/core/author"Hao L."xsd:string
http://purl.uniprot.org/citations/23696660http://purl.uniprot.org/core/author"Flavell R.A."xsd:string
http://purl.uniprot.org/citations/23696660http://purl.uniprot.org/core/author"Flavell R.A."xsd:string
http://purl.uniprot.org/citations/23696660http://purl.uniprot.org/core/author"Jin C."xsd:string
http://purl.uniprot.org/citations/23696660http://purl.uniprot.org/core/author"Jin C."xsd:string
http://purl.uniprot.org/citations/23696660http://purl.uniprot.org/core/author"Huber S."xsd:string
http://purl.uniprot.org/citations/23696660http://purl.uniprot.org/core/author"Huber S."xsd:string
http://purl.uniprot.org/citations/23696660http://purl.uniprot.org/core/author"Eisenbarth S.C."xsd:string
http://purl.uniprot.org/citations/23696660http://purl.uniprot.org/core/author"Eisenbarth S.C."xsd:string
http://purl.uniprot.org/citations/23696660http://purl.uniprot.org/core/author"Elinav E."xsd:string
http://purl.uniprot.org/citations/23696660http://purl.uniprot.org/core/author"Elinav E."xsd:string
http://purl.uniprot.org/citations/23696660http://purl.uniprot.org/core/author"Strowig T."xsd:string
http://purl.uniprot.org/citations/23696660http://purl.uniprot.org/core/author"Strowig T."xsd:string
http://purl.uniprot.org/citations/23696660http://purl.uniprot.org/core/author"Wunderlich C."xsd:string
http://purl.uniprot.org/citations/23696660http://purl.uniprot.org/core/author"Wunderlich C."xsd:string
http://purl.uniprot.org/citations/23696660http://purl.uniprot.org/core/author"Hafemann A."xsd:string
http://purl.uniprot.org/citations/23696660http://purl.uniprot.org/core/author"Hafemann A."xsd:string