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dc.contributor.authorMorris, MA
dc.contributor.authorLaverick, L
dc.contributor.authorWei, W
dc.contributor.authorDavis, AM
dc.contributor.authorO'Neill, S
dc.contributor.authorWood, L
dc.contributor.authorWright, J
dc.contributor.authorDawson, CW
dc.contributor.authorYoung, LS
dc.date.accessioned2020-12-17T03:45:30Z
dc.date.available2020-12-17T03:45:30Z
dc.date.issued2018-05-01
dc.identifierpii: cancers10050130
dc.identifier.citationMorris, M. A., Laverick, L., Wei, W., Davis, A. M., O'Neill, S., Wood, L., Wright, J., Dawson, C. W. & Young, L. S. (2018). The EBV-Encoded Oncoprotein, LMP1, Induces an Epithelial-to-Mesenchymal Transition (EMT) via Its CTAR1 Domain through Integrin-Mediated ERK-MAPK Signalling. CANCERS, 10 (5), https://doi.org/10.3390/cancers10050130.
dc.identifier.issn2072-6694
dc.identifier.urihttp://hdl.handle.net/11343/255018
dc.description.abstractThe Epstein⁻Barr virus (EBV)-encoded latent membrane protein 1 (LMP1) oncogene can induce profound effects on epithelial growth and differentiation including many of the features of the epithelial-to-mesenchymal transition (EMT). To better characterise these effects, we used the well-defined Madin Darby Canine Kidney (MDCK) epithelial cell model and found that LMP1 expression in these cells induces EMT as defined by characteristic morphological changes accompanied by loss of E-cadherin, desmosomal cadherin and tight junction protein expression. The induction of the EMT phenotype required a functional CTAR1 domain of LMP1 and studies using pharmacological inhibitors revealed contributions from signalling pathways commonly induced by integrin⁻ligand interactions: extracellular signal-regulated kinases/mitogen-activated protein kinases (ERK-MAPK), PI3-Kinase and tyrosine kinases, but not transforming growth factor beta (TGFβ). More detailed analysis implicated the CTAR1-mediated induction of Slug and Twist in LMP1-induced EMT. A key role for β1 integrin signalling in LMP1-mediated ERK-MAPK and focal adhesion kianse (FAK) phosphorylation was observed, and β1 integrin activation was found to enhance LMP1-induced cell viability and survival. These findings support an important role for LMP1 in disease pathogenesis through transcriptional reprogramming that enhances tumour cell survival and leads to a more invasive, metastatic phenotype.
dc.languageEnglish
dc.publisherMDPI
dc.titleThe EBV-Encoded Oncoprotein, LMP1, Induces an Epithelial-to-Mesenchymal Transition (EMT) via Its CTAR1 Domain through Integrin-Mediated ERK-MAPK Signalling
dc.typeJournal Article
dc.identifier.doi10.3390/cancers10050130
melbourne.affiliation.departmentMedicine and Radiology
melbourne.source.titleCancers
melbourne.source.volume10
melbourne.source.issue5
dc.rights.licenseCC BY
melbourne.elementsid1328608
melbourne.contributor.authorLaverick, Louise
dc.identifier.eissn2072-6694
melbourne.accessrightsOpen Access


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