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dc.contributor.authorCovert, Hunter
dc.contributor.authorMellor Liliana F, Liliana F 
dc.contributor.authorWolf, Cody L
dc.contributor.authorAnkenbrandt, Nicole
dc.contributor.authorEmathinger, Jacqueline M
dc.contributor.authorTawara, Ken
dc.contributor.authorOxford, Julie Thom
dc.contributor.authorJorcyk, Cheryl L
dc.date.accessioned2020-03-30T14:25:21Z
dc.date.available2020-03-30T14:25:21Z
dc.date.issued2019-08-15
dc.identifier.citationCancer Manag Res. 2019;11:7721-7737.es_ES
dc.identifier.issn1179-1322es_ES
dc.identifier.urihttp://hdl.handle.net/20.500.12105/9370
dc.description.abstractBackground: Hormone receptor status in human breast cancer cells is a strong indicator of the aggressiveness of a tumor. Triple negative breast cancers (TNBC) are aggressive, difficult to treat, and contribute to high incidences of metastasis by possessing characteristics such as increased tumor cell migration and a large presence of the transmembrane protein, cluster of differentiation 44 (CD44) on the cell membrane. Estrogen receptor-positive (ER+) cells are less aggressive and do not migrate until undergoing an epithelial-mesenchymal transition (EMT). Methods: The relationship between EMT and CD44 during metastatic events is assessed by observing changes in EMT markers, tumor cell detachment, and migration following cytokine treatment on both parental and CD44 knockdown human breast tumor cells. Results: ER+ T47D and MCF-7 human breast cancer cells treated with OSM demonstrate increased CD44 expression and CD44 cleavage. Conversely, ER- MDA-MB-231 human breast cancer cells do not show a change in CD44 expression nor undergo EMT in the presence of OSM. In ER+ cells, knockdown expression of CD44 by shRNA did not prevent EMT but did change metastatic processes such as cellular detachment and migration. OSM-induced migration was decreased in both ER+ and ER- cells with shCD44 cells compared to control cells, while the promotion of tumor cell detachment by OSM was decreased in ER+ MCF7-shCD44 cells, as compared to control cells. Interestingly, OSM-induced detachment in ER- MDA-MB-231-shCD44 cells that normally don't detach at significant rates. Conclusion: OSM promotes both EMT and tumor cell detachment in ER+ breast cancer cells. Yet, CD44 knockdown did not affect OSM-induced EMT in these cells, while independently decreasing OSM-induced cell detachment. These results suggest that regulation of CD44 by OSM is important for at least part of the metastatic cascade in ER+ breast cancer.es_ES
dc.description.sponsorshipThe following people have contributed to this work in more ways than one. Raquel Brown provided great insight and technical experience for immunofluorescent imaging. Hannah Scott provided data analysis and contributed to the growth and propagation of cells used for this study. This study was partially funded by the following grants: NIH/NCI R15CA137510, NIH/NCRR P20RR016454, NIH/NIGMS P20GM103408, NIH/NIGMS P20GM109095, Susan G. Komen Foundation KG100513, and American Cancer Society RSG-09-276-01-CSM.es_ES
dc.language.isoenges_ES
dc.publisherDove Medical Press es_ES
dc.relation.isversionofPublisher's versiones_ES
dc.rights.urihttp://creativecommons.org/licenses/by-nc-sa/4.0/*
dc.subjectOncostatin Mes_ES
dc.subjectbreast tumor metastasises_ES
dc.subjectcluster of differentiation 44es_ES
dc.subjectepithelial to mesenchymal transitiones_ES
dc.titleOSM-induced CD44 contributes to breast cancer metastatic potential through cell detachment but not epithelial-mesenchymal transitiones_ES
dc.typeArtículoes_ES
dc.rights.licenseAtribución-NoComercial-CompartirIgual 4.0 Internacional*
dc.identifier.pubmedID31496817es_ES
dc.format.volume11es_ES
dc.format.page7721-7737es_ES
dc.identifier.doi10.2147/CMAR.S208721es_ES
dc.contributor.funderUnited States Department of Health & Human Services National Institutes of Health (NIH) - USA
dc.contributor.funderNIH National Institute of General Medical Sciences (NIGMS)
dc.contributor.funderNIH National Cancer Institute (NCI)
dc.contributor.funderSusan G. Komen Breast Cancer Foundation
dc.contributor.funderAmerican Cancer Society
dc.description.peerreviewedes_ES
dc.relation.publisherversionhttps://doi.org/10.2147/CMAR.S208721es_ES
dc.identifier.journalCancer management and researches_ES
dc.repisalud.institucionCNIOes_ES
dc.repisalud.orgCNIOCNIO::Unidades técnicas::Unidad de Investigación Clínica de Cáncer de Mamaes_ES
dc.rights.accessRightsinfo:eu-repo/semantics/openAccesses_ES


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Atribución-NoComercial-CompartirIgual 4.0 Internacional
This item is licensed under a: Atribución-NoComercial-CompartirIgual 4.0 Internacional