Cyclin D1, Id1 and EMT in breast cancer.
dc.contributor.author | Tobin, Nicholas P | |
dc.contributor.author | Sims, A H | |
dc.contributor.author | Lundgren, Katja L | |
dc.contributor.author | Lehn, Sophie | |
dc.contributor.author | Landberg, Göran | |
dc.date.accessioned | 2012-04-20T08:39:41Z | |
dc.date.available | 2012-04-20T08:39:41Z | |
dc.date.issued | 2011 | |
dc.identifier.citation | Cyclin D1, Id1 and EMT in breast cancer. 2011, 11:417 BMC Cancer | en_GB |
dc.identifier.issn | 1471-2407 | |
dc.identifier.pmid | 21955753 | |
dc.identifier.doi | 10.1186/1471-2407-11-417 | |
dc.identifier.uri | http://hdl.handle.net/10541/219551 | |
dc.description.abstract | Cyclin 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.iso | en | en |
dc.rights | Archived with thanks to BMC cancer | en_GB |
dc.subject.mesh | Breast Neoplasms | |
dc.subject.mesh | Cell Line, Tumor | |
dc.subject.mesh | Cell Movement | |
dc.subject.mesh | Cluster Analysis | |
dc.subject.mesh | Cyclin D1 | |
dc.subject.mesh | Epithelial-Mesenchymal Transition | |
dc.subject.mesh | Female | |
dc.subject.mesh | Gene Expression Profiling | |
dc.subject.mesh | Gene Expression Regulation, Neoplastic | |
dc.subject.mesh | Gene Silencing | |
dc.subject.mesh | Humans | |
dc.subject.mesh | Inhibitor of Differentiation Protein 1 | |
dc.subject.mesh | Prognosis | |
dc.subject.mesh | Recurrence | |
dc.subject.mesh | Risk | |
dc.subject.mesh | Transforming Growth Factor beta | |
dc.title | Cyclin D1, Id1 and EMT in breast cancer. | en |
dc.type | Article | en |
dc.contributor.department | University of Manchester, Manchester, UK. | en_GB |
dc.identifier.journal | BMC Cancer | en_GB |
html.description.abstract | Cyclin 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. |