KOPS - Das Institutionelle Repositorium der Universität Konstanz

Persistent STAT3 activation in colon cancer is associated with enhanced cell proliferation and tumor growth

Persistent STAT3 activation in colon cancer is associated with enhanced cell proliferation and tumor growth

Zitieren

Dateien zu dieser Ressource

Dateien Größe Format Anzeige

Zu diesem Dokument gibt es keine Dateien.

CORVINUS, Florian M., Carina ORTH, Richard MORIGGL, Svetlana A. TSAREVA, Stefan WAGNER, Edith B. PFITZNER, Daniela BAUS, Roland KAUFMANN, Lukas A. HUBERB, Kurt ZATLOUKAL, Hartmut BEUG, Peter ÖHLSCHLÄGER, Alexander SCHÜTZ, Karl-Jürgen HALBHUBER, Karlheinz FRIEDRICH, 2005. Persistent STAT3 activation in colon cancer is associated with enhanced cell proliferation and tumor growth. In: Neoplasia. 7(6), pp. 545-555. ISSN 1476-5586. Available under: doi: 10.1593/neo.04571

@article{Corvinus2005Persi-17504, title={Persistent STAT3 activation in colon cancer is associated with enhanced cell proliferation and tumor growth}, year={2005}, doi={10.1593/neo.04571}, number={6}, volume={7}, issn={1476-5586}, journal={Neoplasia}, pages={545--555}, author={Corvinus, Florian M. and Orth, Carina and Moriggl, Richard and Tsareva, Svetlana A. and Wagner, Stefan and Pfitzner, Edith B. and Baus, Daniela and Kaufmann, Roland and Huberb, Lukas A. and Zatloukal, Kurt and Beug, Hartmut and Öhlschläger, Peter and Schütz, Alexander and Halbhuber, Karl-Jürgen and Friedrich, Karlheinz} }

<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/123456789/17504"> <dc:contributor>Beug, Hartmut</dc:contributor> <dc:contributor>Halbhuber, Karl-Jürgen</dc:contributor> <dcterms:issued>2005</dcterms:issued> <void:sparqlEndpoint rdf:resource="http://localhost/fuseki/dspace/sparql"/> <dc:creator>Öhlschläger, Peter</dc:creator> <dc:date rdf:datatype="http://www.w3.org/2001/XMLSchema#dateTime">2012-01-18T09:24:18Z</dc:date> <dc:creator>Moriggl, Richard</dc:creator> <dc:rights>deposit-license</dc:rights> <dc:contributor>Wagner, Stefan</dc:contributor> <dc:contributor>Schütz, Alexander</dc:contributor> <dcterms:rights rdf:resource="http://nbn-resolving.org/urn:nbn:de:bsz:352-20140905103605204-4002607-1"/> <dc:contributor>Zatloukal, Kurt</dc:contributor> <dc:contributor>Baus, Daniela</dc:contributor> <bibo:uri rdf:resource="http://kops.uni-konstanz.de/handle/123456789/17504"/> <dc:contributor>Tsareva, Svetlana A.</dc:contributor> <dcterms:available rdf:datatype="http://www.w3.org/2001/XMLSchema#dateTime">2012-01-18T09:24:18Z</dcterms:available> <dc:contributor>Huberb, Lukas A.</dc:contributor> <dc:contributor>Öhlschläger, Peter</dc:contributor> <dc:creator>Zatloukal, Kurt</dc:creator> <dc:creator>Tsareva, Svetlana A.</dc:creator> <dcterms:abstract xml:lang="eng">Colorectal carcinoma (CRC) is a major cause of morbidity and mortality in Western countries. It has so far been molecularly defined mainly by alterations of the Wnt pathway. We show here for the first time that aberrant activities of the signal transducer and activator of transcription STAT3 actively contribute to this malignancy and, thus, are a potential therapeutic target for CRC. Constitutive STAT3 activity was found to be abundant in dedifferentiated cancer cells and infiltrating lymphocytes of CRC samples, but not in non-neoplastic colon epithelium. Cell lines derived from malignant colorectal tumors lost persistent STAT3 activity in culture. However, implantation of colon carcinoma cells into nude mice resulted in restoration of STAT3 activity, suggesting a role of an extracellular stimulus within the tumor microenvironment as a trigger for STAT activation. STAT3 activity in CRC cells triggered through interleukin-6 or through a constitutively active STAT3 mutant promoted cancer cell multiplication, whereas STAT3 inhibition through a dominant-negative variant impaired IL-6-driven proliferation. Blockade of STAT3 activation in CRC-derived xenograft tumors slowed down their development, arguing for a contribution of STAT3 to colorectal tumor growth.</dcterms:abstract> <dc:creator>Orth, Carina</dc:creator> <dc:contributor>Corvinus, Florian M.</dc:contributor> <dc:creator>Huberb, Lukas A.</dc:creator> <dc:creator>Friedrich, Karlheinz</dc:creator> <dc:contributor>Moriggl, Richard</dc:contributor> <dc:contributor>Friedrich, Karlheinz</dc:contributor> <dc:creator>Baus, Daniela</dc:creator> <dc:creator>Corvinus, Florian M.</dc:creator> <dc:creator>Pfitzner, Edith B.</dc:creator> <foaf:homepage rdf:resource="http://localhost:8080/jspui"/> <dcterms:isPartOf rdf:resource="https://kops.uni-konstanz.de/rdf/resource/123456789/28"/> <dc:creator>Schütz, Alexander</dc:creator> <dc:contributor>Orth, Carina</dc:contributor> <dc:creator>Wagner, Stefan</dc:creator> <dcterms:title>Persistent STAT3 activation in colon cancer is associated with enhanced cell proliferation and tumor growth</dcterms:title> <dcterms:bibliographicCitation>Publ. in: Neoplasia ; 7 (2005), 6. - S. 545–555</dcterms:bibliographicCitation> <dc:creator>Kaufmann, Roland</dc:creator> <dc:contributor>Pfitzner, Edith B.</dc:contributor> <dc:creator>Halbhuber, Karl-Jürgen</dc:creator> <dc:creator>Beug, Hartmut</dc:creator> <dc:contributor>Kaufmann, Roland</dc:contributor> <dc:language>eng</dc:language> <dspace:isPartOfCollection rdf:resource="https://kops.uni-konstanz.de/rdf/resource/123456789/28"/> </rdf:Description> </rdf:RDF>

Das Dokument erscheint in:

KOPS Suche


Stöbern

Mein Benutzerkonto