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dc.contributor.authorKe, Xi-Songen_US
dc.contributor.authorQu, Yien_US
dc.contributor.authorGoldfinger, Naomien_US
dc.contributor.authorRostad, Karien_US
dc.contributor.authorHovland, Randien_US
dc.contributor.authorAkslen, Lars A.en_US
dc.contributor.authorRotter, Vardaen_US
dc.contributor.authorØyan, Anne Margreteen_US
dc.contributor.authorKalland, Karl-Henningen_US
dc.date.accessioned2013-06-23T12:01:56Z
dc.date.available2013-06-23T12:01:56Z
dc.date.issued2008-10-13eng
dc.PublishedPLoS ONE 3(10):e3368eng
dc.identifier.issn1932-6203
dc.identifier.urihttps://hdl.handle.net/1956/6715
dc.description.abstractBackground: Epithelial to mesenchymal transition (EMT) has been connected with cancer progression in vivo and the generation of more aggressive cancer cell lines in vitro. EMT has been induced in prostate cancer cell lines, but has previously not been shown in primary prostate cells. The role of EMT in malignant transformation has not been clarified. Methodology/Principal Findings: In a transformation experiment when selecting for cells with loss of contact inhibition, the immortalized prostate primary epithelial cell line, EP156T, was observed to undergo EMT accompanied by loss of contact inhibition after about 12 weeks in continuous culture. The changed new cells were named EPT1. EMT of EPT1 was characterized by striking morphological changes and increased invasion and migration compared with the original EP156T cells. Gene expression profiling showed extensively decreased epithelial markers and increased mesenchymal markers in EPT1 cells, as well as pronounced switches of gene expression modules involved in cell adhesion and attachment. Transformation assays showed that EPT1 cells were sensitive to serum or growth factor withdrawal. Most importantly, EPT1 cells were not able to grow in an anchorage-independent way in soft agar, which is considered a critical feature of malignant transformation. Conclusions/Significance: This work for the first time established an EMT model from primary prostate cells. The results show that EMT can be activated as a coordinated gene expression program in association with early steps of transformation. The model allows a clearer identification of the molecular mechanisms of EMT and its potential role in malignant transformation.en_US
dc.language.isoengeng
dc.publisherPublic Library of Scienceeng
dc.relation.ispartof<a href="http://hdl.handle.net/1956/6716" target="blank">Generation of a stepwise prostate carcinogenesis model</a>eng
dc.rightsAttribution CC BYeng
dc.rights.urihttp://creativecommons.org/licenses/by/2.5/eng
dc.titleEpithelial to Mesenchymal Transition of a Primary Prostate Cell Line with Switches of Cell Adhesion Modules but without Malignant Transformationen_US
dc.typePeer reviewed
dc.typeJournal article
dc.description.versionpublishedVersionen_US
dc.rights.holderCopyright 2008 Ke et al.
dc.identifier.doihttps://doi.org/10.1371/journal.pone.0003368
dc.source.journalPLoS ONE
dc.source.403
dc.source.1410


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