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dc.contributor.authorSkalamera, Dubravka
dc.contributor.authorDahmer-Heath, Mareike
dc.contributor.authorStevenson, Alexander J
dc.contributor.authorPinto, Cletus
dc.contributor.authorShah, Esha T
dc.contributor.authorDaignault, Sheena M
dc.contributor.authorSaid, Nur Akmarina BM
dc.contributor.authorDavis, Melissa
dc.contributor.authorHaass, Nikolas K
dc.contributor.authorWilliams, Elizabeth D
dc.contributor.authorHollier, Brett G
dc.contributor.authorThompson, Erik W
dc.contributor.authorGabrielli, Brian
dc.contributor.authorGonda, Thomas J
dc.date.accessioned2020-02-17T02:39:33Z
dc.date.available2020-02-17T02:39:33Z
dc.date.issued2016
dc.identifier.issn1949-2553
dc.identifier.doi10.18632/oncotarget.11314
dc.identifier.urihttp://hdl.handle.net/10072/391561
dc.description.abstractEpithelial to mesenchymal transition (EMT) is a developmental program that has been implicated in progression, metastasis and therapeutic resistance of some carcinomas. To identify genes whose overexpression drives EMT, we screened a lentiviral expression library of 17000 human open reading frames (ORFs) using high-content imaging to quantitate cytoplasmic vimentin. Hits capable of increasing vimentin in the mammary carcinoma-derived cell line MDA-MB-468 were confirmed in the non-tumorigenic breast-epithelial cell line MCF10A. When overexpressed in this model, they increased the rate of cell invasion through Matrigel™, induced mesenchymal marker expression and reduced expression of the epithelial marker E-cadherin. In gene-expression datasets derived from breast cancer patients, the expression of several novel genes correlated with expression of known EMT marker genes, indicating their in vivo relevance. As EMT-associated properties are thought to contribute in several ways to cancer progression, genes identified in this study may represent novel targets for anti-cancer therapy.
dc.description.peerreviewedYes
dc.languageEnglish
dc.language.isoeng
dc.publisherImpact Journals, LLC
dc.relation.ispartofpagefrom61000
dc.relation.ispartofpageto61020
dc.relation.ispartofissue38
dc.relation.ispartofjournalOncotarget
dc.relation.ispartofvolume7
dc.subject.fieldofresearchOncology and Carcinogenesis
dc.subject.fieldofresearchcode1112
dc.subject.keywordsScience & Technology
dc.subject.keywordsLife Sciences & Biomedicine
dc.subject.keywordsOncology
dc.subject.keywordsCell Biology
dc.subject.keywordshigh-content-screening
dc.titleGenome-wide gain-of-function screen for genes that induce epithelial-to-mesenchymal transition in breast cancer
dc.typeJournal article
dc.type.descriptionC1 - Articles
dcterms.bibliographicCitationSkalamera, D; Dahmer-Heath, M; Stevenson, AJ; Pinto, C; Shah, ET; Daignault, SM; Said, NABM; Davis, M; Haass, NK; Williams, ED; Hollier, BG; Thompson, EW; Gabrielli, B; Gonda, TJ, Genome-wide gain-of-function screen for genes that induce epithelial-to-mesenchymal transition in breast cancer, Oncotarget, 2016, 7 (38), pp. 61000-61020
dcterms.dateAccepted2016-07-27
dcterms.licensehttp://creativecommons.org/licenses/by/3.0/
dc.date.updated2020-02-17T02:37:24Z
dc.description.versionVersion of Record (VoR)
gro.rights.copyright© 2016 Skalamera et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License 3.0 (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
gro.hasfulltextFull Text
gro.griffith.authorGabrielli, Brian


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