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dc.contributor.authorJohnstone, Cameron N-
dc.contributor.authorPattison, Andrew D-
dc.contributor.authorHarrison, Paul F-
dc.contributor.authorPowell, David R-
dc.contributor.authorLock, Peter-
dc.contributor.authorErnst, Matthias-
dc.contributor.authorAnderson, Robin L-
dc.contributor.authorBeilharz, Traude H-
dc.identifier.citationInternational journal of cancer 2020; 147(1): 230-243-
dc.description.abstractTriple-negative breast cancer (TNBC) represents 10-20% of all human ductal adenocarcinomas and has a poor prognosis relative to other subtypes, due to the high propensity to develop distant metastases. Hence, new molecular targets for therapeutic intervention are needed for TNBC. We recently conducted a rigorous phenotypic and genomic characterization of four isogenic populations of MDA-MB-231 human triple-negative breast cancer cells that possess a range of intrinsic spontaneous metastatic capacities in vivo, ranging from non-metastatic (MDA-MB-231_ATCC) to highly metastatic to lung, liver, spleen and spine (MDA-MB-231_HM). Gene expression profiling of primary tumours by RNA-Seq identified the fibroblast growth factor homologous factor, FGF13, as highly upregulated in aggressively metastatic MDA-MB-231_HM tumours. Clinically, higher FGF13 mRNA expression was associated with significantly worse relapse free survival in both luminal A and basal-like human breast cancers but was not associated with other clinical variables and was not upregulated in primary tumours relative to normal mammary gland. Stable FGF13 depletion restricted in vitro colony forming ability in MDA-MB-231_HM TNBC cells but not in oestrogen receptor (ER) positive MCF-7 or MDA-MB-361 cells. However, despite augmenting MDA-MB-231_HM cell migration and invasion in vitro, FGF13 suppression almost completely blocked the spontaneous metastasis of MDA-MB-231_HM orthotopic xenografts to both lung and liver while having negligible impact on primary tumour growth. Together, these data indicate that FGF13 may represent a therapeutic target for blocking metastatic outgrowth of certain TNBCs. Further evaluation of the roles of individual FGF13 protein isoforms in progression of the different subtypes of breast cancer is warranted. This article is protected by copyright. All rights reserved.-
dc.subjectmouse model-
dc.subjecttriple-negative breast cancer-
dc.titleFGF13 promotes metastasis of triple-negative breast cancer.-
dc.typeJournal Article-
dc.identifier.journaltitleInternational journal of cancer-
dc.identifier.affiliationLIMS Bioimaging Facility, La Trobe Institute for Molecular Science, La Trobe University, Bundoora, Victoria, Australiaen
dc.identifier.affiliationDepartment of Clinical Pathology, University of Melbourne, Parkville, Victoria, Australiaen
dc.identifier.affiliationOlivia Newton-John Cancer Research Institute, Heidelberg, Victoria, Australiaen
dc.identifier.affiliationSchool of Cancer Medicine, La Trobe University, Bundoora, Victoria, Australiaen
dc.identifier.affiliationDepartment of Biochemistry and Molecular Biology, Monash University, Clayton, Victoria, Australiaen
dc.identifier.affiliationBiomedicine Discovery Institute, Monash University, Clayton, Victoria, Australiaen
dc.identifier.affiliationMonash Bioinformatics Platform, Monash University, Clayton, Victoria, Australiaen
dc.identifier.affiliationCancer Research Division, Peter MacCallum Cancer Centre, Victorian Comprehensive Cancer Centre, Parkville, Victoria, Australiaen
dc.identifier.affiliationSir Peter MacCallum Department of Oncology, University of Melbourne, Parkville, Victoria, Australiaen
dc.type.austinJournal Article-
item.fulltextNo Fulltext-
item.openairetypeJournal Article-
item.cerifentitytypePublications- Newton-John Cancer Research Institute- Newton-John Cancer Research Institute- Newton-John Cancer Research Institute-
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