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dc.contributor.authorDelury, C
dc.contributor.authorHart, Claire A
dc.contributor.authorBrown, Michael D
dc.contributor.authorClarke, Noel W
dc.contributor.authorParkin, E
dc.date.accessioned2016-03-30T09:37:17Zen
dc.date.available2016-03-30T09:37:17Zen
dc.date.issued2016-02-26en
dc.identifier.citationStroma-induced Jagged1 expression drives PC3 prostate cancer cell migration; disparate effects of RIP-generated proteolytic fragments on cell behaviour and Notch signaling. 2016: Biochem Biophys Res Communen
dc.identifier.issn1090-2104en
dc.identifier.pmid26921446en
dc.identifier.doi10.1016/j.bbrc.2016.02.101en
dc.identifier.urihttp://hdl.handle.net/10541/603952en
dc.description.abstractThe Notch ligand Jagged1 is subject to regulated intramembrane proteolysis (RIP) which yields a soluble ectodomain (sJag) and a soluble Jagged1 intracellular domain (JICD). The full-length Jagged1 protein enhances prostate cancer (PCa) cell proliferation and is highly expressed in metastatic cells. However, little is known regarding the mechanisms by which Jagged1 or its RIP-generated fragments might promote PCa bone metastasis. In the current study we show that bone marrow stroma (BMS) induces Jagged1 expression in bone metastatic prostate cancer PC3 cells and that this enhanced expression is mechanistically linked to the promotion of cell migration. We also show that RIP-generated Jagged1 fragments exert disparate effects on PC3 cell behaviour and Notch signaling. In conclusion, the expression of both the full-length ligand and its RIP-generated fragments must be considered in tandem when attempting to regulate Jagged1 as a possible PCa therapy.
dc.languageENGen
dc.language.isoenen
dc.rightsArchived with thanks to Biochemical and biophysical research communicationsen
dc.titleStroma-induced Jagged1 expression drives PC3 prostate cancer cell migration; disparate effects of RIP-generated proteolytic fragments on cell behaviour and Notch signaling.en
dc.typeArticleen
dc.contributor.departmentDivision of Biomedical and Life Sciences, Faculty of Health and Medicine, Lancaster University, Lancaster, LA1 4YQ,en
dc.identifier.journalBiochemical and Biophysical Research Communicationsen
html.description.abstractThe Notch ligand Jagged1 is subject to regulated intramembrane proteolysis (RIP) which yields a soluble ectodomain (sJag) and a soluble Jagged1 intracellular domain (JICD). The full-length Jagged1 protein enhances prostate cancer (PCa) cell proliferation and is highly expressed in metastatic cells. However, little is known regarding the mechanisms by which Jagged1 or its RIP-generated fragments might promote PCa bone metastasis. In the current study we show that bone marrow stroma (BMS) induces Jagged1 expression in bone metastatic prostate cancer PC3 cells and that this enhanced expression is mechanistically linked to the promotion of cell migration. We also show that RIP-generated Jagged1 fragments exert disparate effects on PC3 cell behaviour and Notch signaling. In conclusion, the expression of both the full-length ligand and its RIP-generated fragments must be considered in tandem when attempting to regulate Jagged1 as a possible PCa therapy.


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