Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/16739
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dc.contributor.authorSax, Michael John-
dc.contributor.authorGasch, Christin-
dc.contributor.authorAthota, Vineel Rag-
dc.contributor.authorFreeman, Ruth-
dc.contributor.authorRasighaemi, Parisa-
dc.contributor.authorWestcott, David Elton-
dc.contributor.authorDay, Christopher John-
dc.contributor.authorNikolic, Iva-
dc.contributor.authorElsworth, Benjamin-
dc.contributor.authorWei, Ming-
dc.contributor.authorRogers, Kelly-
dc.contributor.authorSwarbrick, Alexander-
dc.contributor.authorMittal, Vivek-
dc.contributor.authorPouliot, Normand-
dc.contributor.authorMellick, Albert Sleiman-
dc.date2016-12-20-
dc.date.accessioned2017-07-27T03:20:05Z-
dc.date.available2017-07-27T03:20:05Z-
dc.date.issued2016-12-20-
dc.identifier.citationOncotarget 2016; 7(51): 85437-85449en_US
dc.identifier.urihttps://ahro.austin.org.au/austinjspui/handle/1/16739-
dc.description.abstractIt has recently been suggested that the chemokine receptor (CCR5) is required for bone marrow (BM) derived endothelial progenitor cell (EPC) mediated angiogenesis. Here we show that suppression of either cancer cell produced CCL5, or host CCR5 leads to distinctive vascular and tumor growth defects in breast cancer. Surprisingly, CCR5 restoration in the BM alone was not sufficient to rescue the wild type phenotype, suggesting that impaired tumor growth associated with inhibiting CCL5/CCR5 is not due to defects in EPC biology. Instead, to promote angiogenesis cancer cell CCL5 may signal directly to endothelium in the tumor-stroma. In support of this hypothesis, we have also shown: (i) that endothelial cell CCR5 levels increases in response to tumor-conditioned media; (ii) that the amount of CCR5+ tumor vasculature correlates with invasive grade; and (iii) that inhibition of CCL5/CCR5 signaling impairs endothelial cell migration, associated with a decrease in activation of mTOR/AKT pathway members. Finally, we show that treatment with CCR5 antagonist results in less vasculature, impaired tumor growth, reduced metastases and improved survival. Taken as a whole, this work demonstrates that directly inhibiting CCR5 expressing vasculature constitutes a novel strategy for inhibiting angiogenesis and blocking metastatic progression in breast cancer.en_US
dc.subjectAngiogenesisen_US
dc.subjectshRNAien_US
dc.subjectBreast canceren_US
dc.subjectCCL5en_US
dc.subjectCCR5en_US
dc.titleCancer cell CCL5 mediates bone marrow independent angiogenesis in breast canceren_US
dc.typeJournal Articleen_US
dc.identifier.journaltitleOncotargeten_US
dc.identifier.affiliationSchool of Medical Science, Griffith University, Gold Coast, Queensland, Australiaen_US
dc.identifier.affiliationSchool of Medicine, Deakin University, Waurn Ponds, Victoria, Australiaen_US
dc.identifier.affiliationGlycomics Institute, Griffith University, Gold Coast, Queensland, Australiaen_US
dc.identifier.affiliationKinghorn Cancer Centre & Cancer Research Division, Garvan Institute of Medical Research, Darlinghurst, NSW, Australiaen_US
dc.identifier.affiliationSt Vincent’s Clinical School, Faculty of Medicine, University of New South Wales, Kensington, NSW, Australiaen_US
dc.identifier.affiliationCentre for Dynamic Imaging, Walter and Eliza Hall Institute for Medical Research, Parkville, Victoria, Australiaen_US
dc.identifier.affiliationCardiothoracic Surgery and Neuberger Berman Lung Cancer Centre, Weill Cornell Medical College, New York, NY, USAen_US
dc.identifier.affiliationMatrix Microenvironment & Metastasis Laboratory, Olivia Newton-John Cancer Research Institute, Heidelberg, Victoria, Australiaen_US
dc.identifier.affiliationSchool of Cancer Medicine, La Trobe University, Heidelberg, Victoria, Australiaen_US
dc.identifier.affiliationFaculty of Medicine, University of New South Wales, NSW, Australiaen_US
dc.identifier.affiliationSchool of Medicine, Western Sydney University, Campbelltown NSW, Australiaen_US
dc.identifier.affiliationTranslational Oncology Unit, Ingham Institute for Applied Medical Research, Liverpool, NSW, Australiaen_US
dc.identifier.pubmedurihttps://pubmed.ncbi.nlm.nih.gov/27863423en_US
dc.identifier.doi10.18632/oncotarget.13387en_US
dc.type.contentTexten_US
dc.type.austinJournal Articleen_US
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.cerifentitytypePublications-
item.fulltextNo Fulltext-
item.grantfulltextnone-
item.openairetypeJournal Article-
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