Evidence map›Paper›PMID 29723998›Full record

ArticleCancers2018

The EBV-Encoded Oncoprotein, LMP1, Induces an Epithelial-to-Mesenchymal Transition (EMT) via Its CTAR1 Domain through Integrin-Mediated ERK-MAPK Signalling.

Mhairi A Morris, Louise Laverick, Wenbin Wei, Alexandra M Davis, Samantha O'Neill, Liam Wood, Jack Wright, Christopher W Dawson, Lawrence S Young

Open access · goldAbstract read
In one paragraph

Article in Cancers, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.7field-weighted citation impact, top 7% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

28 citing papers in PubMed, 43 citations in OpenAlex.

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  17. Signaling pathways of EBV-induced oncogenesis.Cancer cell international · 2021
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 5 institutions in 2 countries.

Mhairi A MorrisSchool of Sport, Exercise and Health Sciences, Loughborough University, Loughborough LE11 3TU, UK. M.A.Morris@lboro.ac.uk.ORCID 0000-0001-6600-9292
Louise LaverickThe Department of Medicine, Clinical Sciences Building, The Royal Melbourne Hospital, University of Melbourne, Parkville VIC 3010, Australia. louise.laverick@mh.org.au.
Wenbin WeiSheffield Institute of Translational Neuroscience, University of Sheffield, 385a Glossop Road, Sheffield S10 2HQ, UK. w.wei@sheffield.ac.uk.ORCID 0000-0003-1288-6999
Alexandra M DavisFaculty of Health and Life Sciences, De Montfort University, Leicester LE1 9BH, UK. alexandramdavis1@gmail.com.
Samantha O'NeillFaculty of Health and Life Sciences, De Montfort University, Leicester LE1 9BH, UK. samantha.oneill@hotmail.com.
Liam WoodFaculty of Health and Life Sciences, De Montfort University, Leicester LE1 9BH, UK. liamwood94@live.com.
Jack WrightFaculty of Health and Life Sciences, De Montfort University, Leicester LE1 9BH, UK. jackwright71@hotmail.co.uk.
Christopher W DawsonInstitute of Cancer and Genomic Sciences, College of Medicine & Dentistry, University of Birmingham, Birmingham B15 2TT, UK. c.w.dawson@bham.ac.uk.
Lawrence S YoungWarwick Medical School, Gibbet Hill Campus, University of Warwick, Coventry CV4 7AL, UK. L.S.Young@warwick.ac.uk.ORCID 0000-0003-3919-4298
De Montfort University · GBUniversity of Birmingham · GBLoughborough University · GBThe Royal Melbourne Hospital · AUUniversity of Warwick · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

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.

Indexed as

EBVEMTERK-MAPKLMP1NPCPI3-KinaseSrc family kinasesβ1 integrins

Identifiers

PMID29723998
PMCPMC5977103
OpenAlexW2799912985

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.