Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/16773
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dc.contributor.authorJahani-Asl, Arezu-
dc.contributor.authorYin, Hang-
dc.contributor.authorSoleimani, Vahab D-
dc.contributor.authorHaque, Takrima-
dc.contributor.authorLuchman, H Artee-
dc.contributor.authorChang, Natasha C-
dc.contributor.authorSincennes, Marie-Claude-
dc.contributor.authorPuram, Sidharth V-
dc.contributor.authorScott, Andrew M-
dc.contributor.authorLorimer, Ian A J-
dc.contributor.authorPerkins, Theodore J-
dc.contributor.authorLigon, Keith L-
dc.contributor.authorWeiss, Samuel-
dc.contributor.authorRudnicki, Michael A-
dc.contributor.authorBonni, Azad-
dc.date2016-04-25-
dc.date.accessioned2017-08-10T00:34:44Z-
dc.date.available2017-08-10T00:34:44Z-
dc.date.issued2016-06-
dc.identifier.citationNature Neuroscience 2016; 19(6): 798-806en_US
dc.identifier.urihttps://ahro.austin.org.au/austinjspui/handle/1/16773-
dc.description.abstractEGFRvIII-STAT3 signaling is important in glioblastoma pathogenesis. Here, we identified the cytokine receptor OSMR as a direct target gene of the transcription factor STAT3 in mouse astrocytes and human brain tumor stem cells (BTSCs). We found that OSMR functioned as an essential co-receptor for EGFRvIII. OSMR formed a physical complex with EGFRvIII, and depletion of OSMR impaired EGFRvIII-STAT3 signaling. Conversely, pharmacological inhibition of EGFRvIII phosphorylation inhibited the EGFRvIII-OSMR interaction and activation of STAT3. EGFRvIII-OSMR signaling in tumors operated constitutively, whereas EGFR-OSMR signaling in nontumor cells was synergistically activated by the ligands EGF and OSM. Finally, knockdown of OSMR strongly suppressed cell proliferation and tumor growth of mouse glioblastoma cells and human BTSC xenografts in mice, and prolonged the lifespan of these mice. Our findings identify OSMR as a critical regulator of glioblastoma tumor growth that orchestrates a feed-forward signaling mechanism with EGFRvIII and STAT3 to drive tumorigenesis.en_US
dc.subjectBrain Neoplasmsen_US
dc.subjectCell Transformation, Neoplasticen_US
dc.subjectCytokinesen_US
dc.subjectGlioblastomaen_US
dc.subjectSignal Transductionen_US
dc.titleControl of glioblastoma tumorigenesis by feed-forward cytokine signalingen_US
dc.typeJournal Articleen_US
dc.identifier.journaltitleNature Neuroscienceen_US
dc.identifier.affiliationDepartment of Neurobiology, Harvard Medical School, Boston, Massachusetts, USAen_US
dc.identifier.affiliationDepartment of Neuroscience, Washington University School of Medicine, St. Louis, Missouri, USAen_US
dc.identifier.affiliationOttawa Hospital Research Institute, Ottawa, Ontario, Canadaen_US
dc.identifier.affiliationDepartment of Oncology, McGill University, Montreal, Quebec, Canadaen_US
dc.identifier.affiliationLady Davis Institute for Medical Research, Jewish General Hospital, Montreal, Quebec, Canadaen_US
dc.identifier.affiliationDepartment of Cellular and Molecular Medicine, University of Ottawa, Ottawa, Ontario, Canadaen_US
dc.identifier.affiliationDepartment of Biochemistry, University of Georgia, Athens, Georgia, USAen_US
dc.identifier.affiliationMolecular Biology Centre for Molecular Medicine, University of Georgia, Athens, Georgia, USAen_US
dc.identifier.affiliationDepartment of Human Genetics, McGill University, Montreal, Quebec, Canadaen_US
dc.identifier.affiliationDepartment of Cell Biology &Anatomy, University of Calgary, Calgary, Alberta, Canadaen_US
dc.identifier.affiliationOlivia Newton-John Cancer Research Institute, School of Cancer Medicine, La Trobe University, Melbourne, Australiaen_US
dc.identifier.affiliationDepartment of Biochemistry, Microbiology and Immunology, University of Ottawa, Ottawa, Ontario, Canadaen_US
dc.identifier.affiliationDana-Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts, USAen_US
dc.identifier.affiliationDepartment of Pathology, Harvard Medical School, Boston, Massachusetts, USAen_US
dc.identifier.pubmedurihttps://pubmed.ncbi.nlm.nih.gov/27110918en_US
dc.identifier.doi10.1038/nn.4295en_US
dc.type.contentTexten_US
dc.identifier.orcid0000-0002-6656-295Xen_US
dc.type.austinJournal Articleen_US
local.name.researcherScott, Andrew M
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.cerifentitytypePublications-
item.fulltextNo Fulltext-
item.grantfulltextnone-
item.openairetypeJournal Article-
crisitem.author.deptMolecular Imaging and Therapy-
crisitem.author.deptOlivia Newton-John Cancer Research Institute-
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