Show simple item record

dc.contributor.authorCai, L
dc.contributor.authorYe, Y
dc.contributor.authorJiang, Q
dc.contributor.authorChen, Y
dc.contributor.authorLyu, X
dc.contributor.authorLi, J
dc.contributor.authorWang, S
dc.contributor.authorLiu, T
dc.contributor.authorCai, H
dc.contributor.authorYao, K
dc.contributor.authorLi, J-L
dc.contributor.authorLi, X
dc.date.accessioned2016-08-09T14:48:42Z
dc.date.available2016-08-09T14:48:42Z
dc.date.issued2015
dc.identifier.issn2041-1723
dc.identifier.issn2041-1723
dc.identifier.other7353
dc.identifier.urihttp://hdl.handle.net/10026.1/5246
dc.description.abstract

<jats:title>Abstract</jats:title><jats:p>Epstein–Barr virus (EBV), aetiologically linked to nasopharyngeal carcinoma (NPC), is the first human virus found to encode many miRNAs. However, how these viral miRNAs precisely regulate the tumour metastasis in NPC remains obscure. Here we report that EBV-miR-BART1 is highly expressed in NPC and closely associated with pathological and advanced clinical stages of NPC. Alteration of EBV-miR-BART1 expression results in an increase in migration and invasion of NPC cells <jats:italic>in vitro</jats:italic> and causes tumour metastasis <jats:italic>in vivo</jats:italic>. Mechanistically, EBV-miR-BART1 directly targets the cellular tumour suppressor PTEN. Reduction of PTEN dosage by EBV-miR-BART1 activates PTEN-dependent pathways including PI3K-Akt, FAK-p130<jats:sup>Cas</jats:sup> and Shc-MAPK/ERK1/2 signalling, drives EMT, and consequently increases migration, invasion and metastasis of NPC cells. Reconstitution of PTEN rescues all phenotypes generated by EBV-miR-BART1, highlighting the role of PTEN in EBV-miR-BART-driven metastasis in NPC. Our findings provide new insights into the metastasis of NPC regulated by EBV and advocate for developing clinical intervention strategies against NPC.</jats:p>

dc.format.extent7353-
dc.format.mediumElectronic
dc.languageen
dc.language.isoeng
dc.publisherSpringer Science and Business Media LLC
dc.subjectAdult
dc.subjectAnimals
dc.subjectBlotting, Western
dc.subjectCarcinoma
dc.subjectCarcinoma, Squamous Cell
dc.subjectCell Line, Tumor
dc.subjectFemale
dc.subjectGene Expression Regulation, Neoplastic
dc.subjectHEK293 Cells
dc.subjectHead and Neck Neoplasms
dc.subjectHerpesvirus 4, Human
dc.subjectHumans
dc.subjectImmunohistochemistry
dc.subjectMale
dc.subjectMice
dc.subjectMice, Nude
dc.subjectMicroRNAs
dc.subjectNasopharyngeal Carcinoma
dc.subjectNasopharyngeal Neoplasms
dc.subjectNeoplasm Metastasis
dc.subjectNeoplasm Transplantation
dc.subjectPTEN Phosphohydrolase
dc.subjectRNA, Viral
dc.subjectReal-Time Polymerase Chain Reaction
dc.subjectSignal Transduction
dc.subjectSquamous Cell Carcinoma of Head and Neck
dc.titleEpstein–Barr virus-encoded microRNA BART1 induces tumour metastasis by regulating PTEN-dependent pathways in nasopharyngeal carcinoma
dc.typejournal-article
dc.typeArticle
plymouth.author-urlhttps://www.ncbi.nlm.nih.gov/pubmed/26135619
plymouth.issue1
plymouth.volume6
plymouth.publisher-urlhttp://dx.doi.org/10.1038/ncomms8353
plymouth.publication-statusPublished online
plymouth.journalNature Communications
dc.identifier.doi10.1038/ncomms8353
plymouth.organisational-group/Plymouth
plymouth.organisational-group/Plymouth/REF 2021 Researchers by UoA
plymouth.organisational-group/Plymouth/REF 2021 Researchers by UoA/UoA01 Clinical Medicine
plymouth.organisational-group/Plymouth/REF 2021 Researchers by UoA/UoA01 Clinical Medicine/UoA01 Clinical Medicine
dc.publisher.placeEngland
dcterms.dateAccepted2015-04-29
dc.identifier.eissn2041-1723
dc.rights.embargoperiodNot known
rioxxterms.versionofrecord10.1038/ncomms8353
rioxxterms.licenseref.urihttp://www.rioxx.net/licenses/all-rights-reserved
rioxxterms.licenseref.startdate2015-07-02
rioxxterms.typeJournal Article/Review


Files in this item

Thumbnail
Thumbnail

This item appears in the following Collection(s)

Show simple item record


All items in PEARL are protected by copyright law.
Author manuscripts deposited to comply with open access mandates are made available in accordance with publisher policies. Please cite only the published version using the details provided on the item record or document. In the absence of an open licence (e.g. Creative Commons), permissions for further reuse of content should be sought from the publisher or author.
Theme by 
Atmire NV