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The EBV-encoded oncoprotein, LMP1, induces an Epithelial-to-Mesenchymal Transition (EMT) via Its CTAR1 domain through integrin-mediated ERK-MAPK signalling
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Morris, Mhairi, Laverick, Louise, Wei, Wenbin, Davis, Alexandra, O’Neill, Samantha, Wood, Liam, Wright, Jack, Dawson, Christopher and Young, Lawrence (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). p. 130. doi:10.3390/cancers10050130 ISSN 2072-6694.
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Official URL: http://dx.doi.org/10.3390/cancers10050130
Abstract
The 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
| Item Type: | Journal Article | ||||||
|---|---|---|---|---|---|---|---|
| Divisions: | Faculty of Science, Engineering and Medicine > Medicine > Warwick Medical School | ||||||
| Journal or Publication Title: | Cancers | ||||||
| Publisher: | MDPI | ||||||
| ISSN: | 2072-6694 | ||||||
| Official Date: | 1 May 2018 | ||||||
| Dates: |
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| Volume: | 10 | ||||||
| Number: | 5 | ||||||
| Page Range: | p. 130 | ||||||
| DOI: | 10.3390/cancers10050130 | ||||||
| Status: | Peer Reviewed | ||||||
| Publication Status: | Published | ||||||
| Access rights to Published version: | Open Access (Creative Commons) |
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