http://purl.uniprot.org/citations/37260355 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
http://purl.uniprot.org/citations/37260355 | http://www.w3.org/2000/01/rdf-schema#comment | "Protein tyrosine phosphatase receptor zeta 1 (PTPRZ1) is a transmembrane tyrosine phosphatase (TP) expressed in endothelial cells and required for stimulation of cell migration by vascular endothelial growth factor A165 (VEGFA165 ) and pleiotrophin (PTN). It is also over or under-expressed in various tumor types. In this study, we used genetically engineered Ptprz1-/- and Ptprz1+/+ mice to study mechanistic aspects of PTPRZ1 involvement in angiogenesis and investigate its role in lung adenocarcinoma (LUAD) growth. Ptprz1-/- lung microvascular endothelial cells (LMVEC) have increased angiogenic features compared with Ptprz1+/+ LMVEC, in line with the increased lung angiogenesis and the enhanced chemically induced LUAD growth in Ptprz1-/- compared with Ptprz1+/+ mice. In LUAD cells isolated from the lungs of urethane-treated mice, PTPRZ1 TP inhibition also enhanced proliferation and migration. Expression of beta 3 (β3 ) integrin is decreased in Ptprz1-/- LMVEC, linked to enhanced VEGF receptor 2 (VEGFR2), c-Met tyrosine kinase (TK) and Akt kinase activities. However, only c-Met and Akt seem responsible for the enhanced endothelial cell activation in vitro and LUAD growth and angiogenesis in vivo in Ptprz1-/- mice. A selective PTPRZ1 TP inhibitor, VEGFA165 and PTN also activate c-Met and Akt in a PTPRZ1-dependent manner in endothelial cells, and their stimulatory effects are abolished by the c-Met TK inhibitor (TKI) crizotinib. Altogether, our data suggest that low PTPRZ1 expression is linked to worse LUAD prognosis and response to c-Met TKIs and uncover for the first time the role of PTPRZ1 in mediating c-Met activation by VEGFA and PTN."xsd:string |
http://purl.uniprot.org/citations/37260355 | http://purl.org/dc/terms/identifier | "doi:10.1002/ijc.34564"xsd:string |
http://purl.uniprot.org/citations/37260355 | http://purl.uniprot.org/core/author | "Mikelis C.M."xsd:string |
http://purl.uniprot.org/citations/37260355 | http://purl.uniprot.org/core/author | "Papadimitriou E."xsd:string |
http://purl.uniprot.org/citations/37260355 | http://purl.uniprot.org/core/author | "Marazioti A."xsd:string |
http://purl.uniprot.org/citations/37260355 | http://purl.uniprot.org/core/author | "Herradon G."xsd:string |
http://purl.uniprot.org/citations/37260355 | http://purl.uniprot.org/core/author | "Stathopoulos G.T."xsd:string |
http://purl.uniprot.org/citations/37260355 | http://purl.uniprot.org/core/author | "Gramage E."xsd:string |
http://purl.uniprot.org/citations/37260355 | http://purl.uniprot.org/core/author | "Papadaki E."xsd:string |
http://purl.uniprot.org/citations/37260355 | http://purl.uniprot.org/core/author | "Nikou S."xsd:string |
http://purl.uniprot.org/citations/37260355 | http://purl.uniprot.org/core/author | "Choleva E."xsd:string |
http://purl.uniprot.org/citations/37260355 | http://purl.uniprot.org/core/author | "Akwii R.G."xsd:string |
http://purl.uniprot.org/citations/37260355 | http://purl.uniprot.org/core/author | "Kastana P."xsd:string |
http://purl.uniprot.org/citations/37260355 | http://purl.uniprot.org/core/author | "Ntenekou D."xsd:string |
http://purl.uniprot.org/citations/37260355 | http://purl.uniprot.org/core/author | "Enake M.K."xsd:string |
http://purl.uniprot.org/citations/37260355 | http://purl.uniprot.org/core/author | "Mourkogianni E."xsd:string |
http://purl.uniprot.org/citations/37260355 | http://purl.uniprot.org/core/author | "Xanthopoulos A."xsd:string |
http://purl.uniprot.org/citations/37260355 | http://purl.uniprot.org/core/date | "2023"xsd:gYear |
http://purl.uniprot.org/citations/37260355 | http://purl.uniprot.org/core/name | "Int J Cancer"xsd:string |
http://purl.uniprot.org/citations/37260355 | http://purl.uniprot.org/core/pages | "1051-1066"xsd:string |
http://purl.uniprot.org/citations/37260355 | http://purl.uniprot.org/core/title | "Genetic deletion or tyrosine phosphatase inhibition of PTPRZ1 activates c-Met to up-regulate angiogenesis and lung adenocarcinoma growth."xsd:string |
http://purl.uniprot.org/citations/37260355 | http://purl.uniprot.org/core/volume | "153"xsd:string |
http://purl.uniprot.org/citations/37260355 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/37260355 |
http://purl.uniprot.org/citations/37260355 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/37260355 |