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Inhibition and deficiency of the immunoproteasome subunit LMP7 suppress the development and progression of colorectal carcinoma in mice

Inhibition and deficiency of the immunoproteasome subunit LMP7 suppress the development and progression of colorectal carcinoma in mice

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KÖRNER, Julia, Thomas BRUNNER, Marcus GROETTRUP, 2017. Inhibition and deficiency of the immunoproteasome subunit LMP7 suppress the development and progression of colorectal carcinoma in mice. In: Oncotarget. 8(31), pp. 50873-50888. eISSN 1949-2553. Available under: doi: 10.18632/oncotarget.15141

@article{Korner2017-08-01Inhib-38221, title={Inhibition and deficiency of the immunoproteasome subunit LMP7 suppress the development and progression of colorectal carcinoma in mice}, year={2017}, doi={10.18632/oncotarget.15141}, number={31}, volume={8}, journal={Oncotarget}, author={Körner, Julia and Brunner, Thomas and Groettrup, Marcus} }

<rdf:RDF xmlns:dcterms="http://purl.org/dc/terms/" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:rdf="http://www.w3.org/1999/02/22-rdf-syntax-ns#" xmlns:bibo="http://purl.org/ontology/bibo/" xmlns:dspace="http://digital-repositories.org/ontologies/dspace/0.1.0#" xmlns:foaf="http://xmlns.com/foaf/0.1/" xmlns:void="http://rdfs.org/ns/void#" xmlns:xsd="http://www.w3.org/2001/XMLSchema#" > <rdf:Description rdf:about="https://kops.uni-konstanz.de/rdf/resource/123456789/38221"> <dc:contributor>Brunner, Thomas</dc:contributor> <dspace:hasBitstream rdf:resource="https://kops.uni-konstanz.de/bitstream/123456789/38221/1/Koerner_1-25ea2727fd134ac19.pdf"/> <void:sparqlEndpoint rdf:resource="http://localhost/fuseki/dspace/sparql"/> <dcterms:isPartOf rdf:resource="https://kops.uni-konstanz.de/rdf/resource/123456789/28"/> <dcterms:title>Inhibition and deficiency of the immunoproteasome subunit LMP7 suppress the development and progression of colorectal carcinoma in mice</dcterms:title> <dc:contributor>Körner, Julia</dc:contributor> <dc:creator>Körner, Julia</dc:creator> <dcterms:hasPart rdf:resource="https://kops.uni-konstanz.de/bitstream/123456789/38221/1/Koerner_1-25ea2727fd134ac19.pdf"/> <dcterms:issued>2017-08-01</dcterms:issued> <foaf:homepage rdf:resource="http://localhost:8080/jspui"/> <dspace:isPartOfCollection rdf:resource="https://kops.uni-konstanz.de/rdf/resource/123456789/28"/> <bibo:uri rdf:resource="https://kops.uni-konstanz.de/handle/123456789/38221"/> <dcterms:available rdf:datatype="http://www.w3.org/2001/XMLSchema#dateTime">2017-03-30T09:18:57Z</dcterms:available> <dcterms:abstract xml:lang="eng">New treatment options and drug targets for colorectal carcinoma are a pressing medical need. Inflammation and pro-inflammatory cytokines produced by Th1 and Th17 cells like IL-6, TNF, IL-17 and IL-23 promote the development and growth of colorectal cancer (CRC). The immunoproteasome is a proteasome subtype highly expressed in immune cells but also in the intestine. Since the immunoproteasome promotes Th1 and Th17 differentiation and pro-inflammatory cytokine production, we investigated here whether deficiency or inhibition of the immunoproteasome subunit LMP7 would interfere with CRC development and exacerbation in preventive and therapeutic mouse models. Treatment with the LMP7 inhibitor ONX 0914 blocked tumor initiation and progression in either chemically-induced (AOM/DSS) or transgenic mouse models (ApcMin/+) of colon carcinogenesis. ONX 0914 treatment strongly reduced tumor numbers and CRC-associated loss of body weight while the survival rates were significantly enhanced. Moreover, genetic LMP7 deficiency markedly reduced the tumor burden in AOM/DSS induced wild type and ApcMin/+ mice. In conclusion, we show that the immunoproteasome is involved in CRC development and progression and we identify LMP7 as a new potential drug target for the treatment of CRC.</dcterms:abstract> <dc:creator>Brunner, Thomas</dc:creator> <dc:contributor>Groettrup, Marcus</dc:contributor> <dc:creator>Groettrup, Marcus</dc:creator> <dc:date rdf:datatype="http://www.w3.org/2001/XMLSchema#dateTime">2017-03-30T09:18:57Z</dc:date> <dc:language>eng</dc:language> </rdf:Description> </rdf:RDF>

Dateiabrufe seit 30.03.2017 (Informationen über die Zugriffsstatistik)

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