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http://purl.uniprot.org/citations/23733751http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/23733751http://www.w3.org/2000/01/rdf-schema#comment"Metastatic breast cancer remains the chief cause of cancer-related death among women in the Western world. Although loss of cell-cell adhesion is key to breast cancer progression, little is known about the underlying mechanisms that drive tumor invasion and metastasis. Here, we show that somatic loss of p120-catenin (p120) in a conditional mouse model of noninvasive mammary carcinoma results in formation of stromal-dense tumors that resemble human metaplastic breast cancer and metastasize to lungs and lymph nodes. Loss of p120 in anchorage-dependent breast cancer cell lines strongly promoted anoikis resistance through hypersensitization of growth factor receptor (GFR) signaling. Interestingly, p120 deletion also induced secretion of inflammatory cytokines, a feature that likely underlies the formation of the prometastatic microenvironment in p120-negative mammary carcinomas. Our results establish a preclinical platform to develop tailored intervention regimens that target GFR signals to treat p120-negative metastatic breast cancers."xsd:string
http://purl.uniprot.org/citations/23733751http://purl.org/dc/terms/identifier"doi:10.1158/0008-5472.can-13-0180"xsd:string
http://purl.uniprot.org/citations/23733751http://purl.uniprot.org/core/author"Jonkers J."xsd:string
http://purl.uniprot.org/citations/23733751http://purl.uniprot.org/core/author"Vermeulen J.F."xsd:string
http://purl.uniprot.org/citations/23733751http://purl.uniprot.org/core/author"van Diest P.J."xsd:string
http://purl.uniprot.org/citations/23733751http://purl.uniprot.org/core/author"van der Wall E."xsd:string
http://purl.uniprot.org/citations/23733751http://purl.uniprot.org/core/author"Peeters T."xsd:string
http://purl.uniprot.org/citations/23733751http://purl.uniprot.org/core/author"van der Groep P."xsd:string
http://purl.uniprot.org/citations/23733751http://purl.uniprot.org/core/author"Derksen P.W."xsd:string
http://purl.uniprot.org/citations/23733751http://purl.uniprot.org/core/author"Schackmann R.C."xsd:string
http://purl.uniprot.org/citations/23733751http://purl.uniprot.org/core/author"Braumuller T.M."xsd:string
http://purl.uniprot.org/citations/23733751http://purl.uniprot.org/core/author"Vlug E.J."xsd:string
http://purl.uniprot.org/citations/23733751http://purl.uniprot.org/core/author"van Amersfoort M."xsd:string
http://purl.uniprot.org/citations/23733751http://purl.uniprot.org/core/author"Klarenbeek S."xsd:string
http://purl.uniprot.org/citations/23733751http://purl.uniprot.org/core/author"Stelloo S."xsd:string
http://purl.uniprot.org/citations/23733751http://purl.uniprot.org/core/author"Tenhagen M."xsd:string
http://purl.uniprot.org/citations/23733751http://purl.uniprot.org/core/date"2013"xsd:gYear
http://purl.uniprot.org/citations/23733751http://purl.uniprot.org/core/name"Cancer Res"xsd:string
http://purl.uniprot.org/citations/23733751http://purl.uniprot.org/core/pages"4937-4949"xsd:string
http://purl.uniprot.org/citations/23733751http://purl.uniprot.org/core/title"Loss of p120-catenin induces metastatic progression of breast cancer by inducing anoikis resistance and augmenting growth factor receptor signaling."xsd:string
http://purl.uniprot.org/citations/23733751http://purl.uniprot.org/core/volume"73"xsd:string
http://purl.uniprot.org/citations/23733751http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/23733751
http://purl.uniprot.org/citations/23733751http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/23733751
http://purl.uniprot.org/uniprot/#_E9Q8Z5-mappedCitation-23733751http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/23733751