Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/9536
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dc.contributor.authorGallicchio, Marisa Aen
dc.contributor.authorKaun, Christophen
dc.contributor.authorWojta, Johannen
dc.contributor.authorBinder, Bernden
dc.contributor.authorBach, Leon Aen
dc.date.accessioned2015-05-15T22:39:55Z
dc.date.available2015-05-15T22:39:55Z
dc.date.issued2003-10-01en
dc.identifier.citationJournal of Cellular Physiology; 197(1): 131-8en
dc.identifier.govdoc12942549en
dc.identifier.otherPUBMEDen
dc.identifier.urihttp://ahro.austin.org.au/austinjspui/handle/1/9536en
dc.description.abstractUrokinase-type plasminogen activator (uPA) binds to its receptor, uPAR, on the surface of cancer cells, leading to the formation of plasmin. Rhabdomyosarcoma (RMS) cell lines secrete high levels of insulin-like growth factor II (IGF-II), suggesting autocrine IGFs play a major role in the unregulated growth and metastasis of RMS. In vitro, IGF-II and IGF-I increased migration of RD cells to 124+/-9% (P<0.01) and 131+/-8% (P<0.05) of control, respectively. IGF-II-induced migration was abolished by insulin-like growth factor binding protein-6 (IGFBP-6) (P<0.01), a relatively specific inhibitor of IGF-II, and by plasminogen activator inhibitor type 1 (PAI-1) (P<0.05). Aprotinin, a plasmin inhibitor, and mannosamine, which inhibits the synthesis of glycosylphosphatidylinositol (GPI), thereby preventing anchorage of GPI-linked proteins such as uPAR to the cell membrane, also decreased IGF-II- (P<0.05 for both) but not IGF-I-induced migration. [Arg54,Arg55]IGF-II and [Leu27]IGF-II, which preferentially bind to the IGF-I and IGF-II/mannose-6-phosphate receptors (IGF-II/M6PR), respectively, both induced RD cell migration to 146+/-8% (P<0.01) and 120+/-7% (P<0.05) of control, respectively. An anti-uPAR anti-serum reduced IGF-II- and IGF-I-induced migration (P<0.05 for both). An anti-low density lipoprotein-related protein (LRP) anti-serum reduced IGF-I-induced migration (P<0.05). IGF-I and -II both increased specific 125I-single chain uPA (scuPA) binding to RD cells in a dose-dependent manner (P<0.01). These results suggest involvement of the PA/plasmin system in IGF-induced migration and indicate important roles these systems may have in RMS metastasis.en
dc.language.isoenen
dc.subject.otherAprotinin.metabolismen
dc.subject.otherCell Movement.drug effects.physiologyen
dc.subject.otherDose-Response Relationship, Drugen
dc.subject.otherEmbryo, Mammalianen
dc.subject.otherEnzyme-Linked Immunosorbent Assayen
dc.subject.otherHexosamines.metabolismen
dc.subject.otherHumansen
dc.subject.otherInsulin-Like Growth Factor Binding Protein 6.metabolismen
dc.subject.otherInsulin-Like Growth Factor I.metabolismen
dc.subject.otherInsulin-Like Growth Factor II.genetics.metabolismen
dc.subject.otherMutationen
dc.subject.otherPlasminogen Activator Inhibitor 1.biosynthesisen
dc.subject.otherReceptors, Cell Surface.drug effects.metabolismen
dc.subject.otherReceptors, Urokinase Plasminogen Activatoren
dc.subject.otherRhabdomyosarcoma.metabolismen
dc.subject.otherTissue Plasminogen Activator.biosynthesis.drug effectsen
dc.subject.otherTumor Cells, Cultureden
dc.subject.otherUrokinase-Type Plasminogen Activator.drug effects.metabolismen
dc.titleUrokinase type plasminogen activator receptor is involved in insulin-like growth factor-induced migration of rhabdomyosarcoma cells in vitro.en
dc.typeJournal Articleen
dc.identifier.journaltitleJournal of cellular physiologyen
dc.identifier.affiliationDepartment of Medicine, University of Melbourne, Austin and Repatriation Medical Centre (Austin Campus), Heidelberg, Victoria, Australiaen
dc.identifier.doi10.1002/jcp.10352en
dc.description.pages131-8en
dc.relation.urlhttps://pubmed.ncbi.nlm.nih.gov/12942549en
dc.type.austinJournal Articleen
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.grantfulltextnone-
item.openairetypeJournal Article-
item.fulltextNo Fulltext-
item.cerifentitytypePublications-
item.languageiso639-1en-
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