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http://purl.uniprot.org/citations/21249149http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/21249149http://www.w3.org/2000/01/rdf-schema#comment"Members of the BMP and Wnt protein families play a relevant role in physiologic and pathologic bone turnover. Extracellular antagonists are crucial for the modulation of their activity. Lack of expression of the BMP antagonist noggin by osteoinductive, carcinoma-derived cell lines is a determinant of the osteoblast response induced by their bone metastases. In contrast, osteolytic, carcinoma-derived cell lines express noggin constitutively. We hypothesized that cancer cell-derived noggin may contribute to the pathogenesis of osteolytic bone metastasis of solid cancers by repressing bone formation. Intra-osseous xenografts of PC-3 prostate cancer cells induced osteolytic lesions characterized not only by enhanced osteoclast-mediated bone resorption, but also by decreased osteoblast-mediated bone formation. Therefore, in this model, uncoupling of the bone remodeling process contributes to osteolysis. Bone formation was preserved in the osteolytic lesions induced by noggin-silenced PC-3 cells, suggesting that cancer cell-derived noggin interferes with physiologic bone coupling. Furthermore, intra-osseous tumor growth of noggin-silenced PC-3 cells was limited, most probably as a result of the persisting osteoblast activity. This investigation provides new evidence for a model of osteolytic bone metastasis where constitutive secretion of noggin by cancer cells mediates inhibition of bone formation, thereby preventing repair of osteolytic lesions generated by an excess of osteoclast-mediated bone resorption. Therefore, noggin suppression may be a novel strategy for the treatment of osteolytic bone metastases."xsd:string
http://purl.uniprot.org/citations/21249149http://purl.org/dc/terms/identifier"doi:10.1371/journal.pone.0016078"xsd:string
http://purl.uniprot.org/citations/21249149http://purl.uniprot.org/core/author"Cecchini M.G."xsd:string
http://purl.uniprot.org/citations/21249149http://purl.uniprot.org/core/author"Wetterwald A."xsd:string
http://purl.uniprot.org/citations/21249149http://purl.uniprot.org/core/author"Schwaninger R."xsd:string
http://purl.uniprot.org/citations/21249149http://purl.uniprot.org/core/author"Thalmann G.N."xsd:string
http://purl.uniprot.org/citations/21249149http://purl.uniprot.org/core/author"Secondini C."xsd:string
http://purl.uniprot.org/citations/21249149http://purl.uniprot.org/core/date"2011"xsd:gYear
http://purl.uniprot.org/citations/21249149http://purl.uniprot.org/core/name"PLoS One"xsd:string
http://purl.uniprot.org/citations/21249149http://purl.uniprot.org/core/pages"e16078"xsd:string
http://purl.uniprot.org/citations/21249149http://purl.uniprot.org/core/title"The role of the BMP signaling antagonist noggin in the development of prostate cancer osteolytic bone metastasis."xsd:string
http://purl.uniprot.org/citations/21249149http://purl.uniprot.org/core/volume"6"xsd:string
http://purl.uniprot.org/citations/21249149http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/21249149
http://purl.uniprot.org/citations/21249149http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/21249149
http://purl.uniprot.org/uniprot/#_B2RA81-mappedCitation-21249149http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/21249149
http://purl.uniprot.org/uniprot/#_Q13253-mappedCitation-21249149http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/21249149
http://purl.uniprot.org/uniprot/Q13253http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/21249149
http://purl.uniprot.org/uniprot/B2RA81http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/21249149