http://purl.uniprot.org/citations/19556880 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
http://purl.uniprot.org/citations/19556880 | http://www.w3.org/2000/01/rdf-schema#comment | "Vascular endothelial growth factor receptor-3 is a receptor tyrosine kinase that is overexpressed in some human carcinomas, but its role in tumorigenesis has not been fully elucidated. We examined VEGFR-3 expression in normal, nonneoplastic and early stage malignant breast tissues and have shown that VEGFR-3 upregulation in breast cancer preceded tumor cell invasion, suggesting that VEGFR-3 may function as a survival signal. We characterized the biological effects of VEGFR-3 over-expression in human breast cancer cells based on two approaches: gain of function by overexpressing VEGFR-3 in MCF-7 breast cancer cells and loss of function by RNAi-mediated silencing of VEGFR-3 in MCF-7-VEGFR-3 and BT474 cells. VEGFR-3 overexpression increased cellular proliferation by 40% when MCF7-VEGFR-3 cells were compared to parental MCF7 cells, and proliferation was reduced by more than 40% when endogenous VEGFR-3 was downregulated in BT474 cells. VEGFR-3 overexpression promoted a three-fold increase in motility and invasion and both motility and invasion were inhibited by downregulation of VEGFR-3. Furthermore, VEGFR-3 overexpression promoted cellular survival under stress conditions induced by staurosporine treatment and led to anchorage-independent growth. VEGFR-3 overexpression dramatically increased tumor formation in both hormone-dependent and independent xenograft models. With estrogen stimulation, MCF7-VEGFR-3 xenografts were ten times larger than control xenografts. Finally, downregulation of VEGFR-3 expression in both xenograft model cell lines led to a significant reduction of tumor growth. For the first time, we have demonstrated that VEGFR-3 overexpression promotes breast cancer cell proliferation, motility, survival, anchorage-independent growth and tumorogenicity in the absence of ligand expression."xsd:string |
http://purl.uniprot.org/citations/19556880 | http://purl.org/dc/terms/identifier | "doi:10.4161/cc.8.14.9101"xsd:string |
http://purl.uniprot.org/citations/19556880 | http://purl.uniprot.org/core/author | "He D."xsd:string |
http://purl.uniprot.org/citations/19556880 | http://purl.uniprot.org/core/author | "Cance W.G."xsd:string |
http://purl.uniprot.org/citations/19556880 | http://purl.uniprot.org/core/author | "Garces C.A."xsd:string |
http://purl.uniprot.org/citations/19556880 | http://purl.uniprot.org/core/author | "Golubovskaya V.M."xsd:string |
http://purl.uniprot.org/citations/19556880 | http://purl.uniprot.org/core/author | "Kurenova E.V."xsd:string |
http://purl.uniprot.org/citations/19556880 | http://purl.uniprot.org/core/author | "Hunt D.L."xsd:string |
http://purl.uniprot.org/citations/19556880 | http://purl.uniprot.org/core/author | "Massoll N.A."xsd:string |
http://purl.uniprot.org/citations/19556880 | http://purl.uniprot.org/core/author | "Fu A.D."xsd:string |
http://purl.uniprot.org/citations/19556880 | http://purl.uniprot.org/core/date | "2009"xsd:gYear |
http://purl.uniprot.org/citations/19556880 | http://purl.uniprot.org/core/name | "Cell Cycle"xsd:string |
http://purl.uniprot.org/citations/19556880 | http://purl.uniprot.org/core/pages | "2266-2280"xsd:string |
http://purl.uniprot.org/citations/19556880 | http://purl.uniprot.org/core/title | "Vascular endothelial growth factor receptor-3 promotes breast cancer cell proliferation, motility and survival in vitro and tumor formation in vivo."xsd:string |
http://purl.uniprot.org/citations/19556880 | http://purl.uniprot.org/core/volume | "8"xsd:string |
http://purl.uniprot.org/citations/19556880 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/19556880 |
http://purl.uniprot.org/citations/19556880 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/19556880 |
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