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dc.contributor.authorTobin, Nicholas P
dc.contributor.authorSims, A H
dc.contributor.authorLundgren, Katja L
dc.contributor.authorLehn, Sophie
dc.contributor.authorLandberg, Göran
dc.date.accessioned2012-04-20T08:39:41Z
dc.date.available2012-04-20T08:39:41Z
dc.date.issued2011
dc.identifier.citationCyclin D1, Id1 and EMT in breast cancer. 2011, 11:417 BMC Canceren_GB
dc.identifier.issn1471-2407
dc.identifier.pmid21955753
dc.identifier.doi10.1186/1471-2407-11-417
dc.identifier.urihttp://hdl.handle.net/10541/219551
dc.description.abstractCyclin D1 is a well-characterised cell cycle regulator with established oncogenic capabilities. Despite these properties, studies report contrasting links to tumour aggressiveness. It has previously been shown that silencing cyclin D1 increases the migratory capacity of MDA-MB-231 breast cancer cells with concomitant increase in 'inhibitor of differentiation 1' (ID1) gene expression. Id1 is known to be associated with more invasive features of cancer and with the epithelial-mesenchymal transition (EMT). Here, we sought to determine if the increase in cell motility following cyclin D1 silencing was mediated by Id1 and enhanced EMT-features. To further substantiate these findings we aimed to delineate the link between CCND1, ID1 and EMT, as well as clinical properties in primary breast cancer.
dc.language.isoenen
dc.rightsArchived with thanks to BMC canceren_GB
dc.subject.meshBreast Neoplasms
dc.subject.meshCell Line, Tumor
dc.subject.meshCell Movement
dc.subject.meshCluster Analysis
dc.subject.meshCyclin D1
dc.subject.meshEpithelial-Mesenchymal Transition
dc.subject.meshFemale
dc.subject.meshGene Expression Profiling
dc.subject.meshGene Expression Regulation, Neoplastic
dc.subject.meshGene Silencing
dc.subject.meshHumans
dc.subject.meshInhibitor of Differentiation Protein 1
dc.subject.meshPrognosis
dc.subject.meshRecurrence
dc.subject.meshRisk
dc.subject.meshTransforming Growth Factor beta
dc.titleCyclin D1, Id1 and EMT in breast cancer.en
dc.typeArticleen
dc.contributor.departmentUniversity of Manchester, Manchester, UK.en_GB
dc.identifier.journalBMC Canceren_GB
html.description.abstractCyclin D1 is a well-characterised cell cycle regulator with established oncogenic capabilities. Despite these properties, studies report contrasting links to tumour aggressiveness. It has previously been shown that silencing cyclin D1 increases the migratory capacity of MDA-MB-231 breast cancer cells with concomitant increase in 'inhibitor of differentiation 1' (ID1) gene expression. Id1 is known to be associated with more invasive features of cancer and with the epithelial-mesenchymal transition (EMT). Here, we sought to determine if the increase in cell motility following cyclin D1 silencing was mediated by Id1 and enhanced EMT-features. To further substantiate these findings we aimed to delineate the link between CCND1, ID1 and EMT, as well as clinical properties in primary breast cancer.


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