Hypermethylation of MAPK13 promoter in oesophageal squamous cell carcinoma Is associated with loss of p38δ MAPK expression

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dc.contributor.author O'Callaghan, Carol
dc.contributor.author Fanning, Liam J.
dc.contributor.author Barry, Orla P.
dc.date.accessioned 2016-03-09T13:59:33Z
dc.date.available 2016-03-09T13:59:33Z
dc.date.issued 2015-10-23
dc.identifier.citation O CALLAGHAN, C., FANNING, L. & BARRY, O. 2015. Hypermethylation of MAPK13 Promoter in Oesophageal Squamous Cell Carcinoma Is Associated with Loss of p38δ MAPK Expression. Cancers, 7, 0881. http://www.mdpi.com/2072-6694/7/4/0881 en
dc.identifier.volume 7 en
dc.identifier.issued 4 en
dc.identifier.startpage 2124 en
dc.identifier.endpage 2133 en
dc.identifier.issn 2072-6694
dc.identifier.uri http://hdl.handle.net/10468/2426
dc.identifier.doi 10.3390/cancers7040881
dc.description.abstract The loss of tumour suppressor gene function is a hallmark of malignant transformation and can occur by a variety of genetic and/or epigenetic alterations. We have previously characterised p38δ mitogen-activated protein kinase (MAPK) as a tumour suppressor in oesophageal squamous cell carcinoma (OESCC) and outlined how loss of p38δ MAPK expression promotes increased proliferation and migration, as well as reduced chemosensitivity. Our aim was to investigate the underlying molecular causes of loss of p38δ MAPK expression in OESCC. Sequence analysis of DNA from p38δ MAPK positive and p38δ MAPK negative OESCC cell lines was used to investigate potential loss of function causing mutations. Epigenetic control of p38δ expression in OESCC was examined using methylation-specific PCR and sequencing of bisulfite-converted DNA. We did not identify any mutations in the MAPK13 sequence in OESCC cell lines which lack p38δ MAPK expression. However, we identified a differential pattern of methylation between p38δ MAPK positive and p38δ MAPK negative cell lines. We outline here for the first time differential MAPK13 promoter methylation in OESCC. Our results suggest that epigenetic alterations are responsible, in part, for the suppression of p38δ MAPK expression and promotion of tumourigenesis in OESCC. en
dc.description.sponsorship Health Research Board, Ireland (Grant HRA/2009/17) en
dc.format.mimetype application/pdf en
dc.language.iso en en
dc.publisher MDPI AG en
dc.rights © 2015 by the authors; licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons by Attribution (CC-BY) license (http://creativecommons.org/licenses/by/4.0/). en
dc.rights.uri http://creativecommons.org/licenses/by/4.0/ en
dc.subject Epigenetics en
dc.subject Methylation en
dc.subject Oesophageal squamous cell carcinoma en
dc.subject p38δ en
dc.subject MAPK en
dc.subject Mitogen activated protein kinase 13 en
dc.subject p38delta MAPK en
dc.subject Messenger RNA en
dc.subject DNA en
dc.title Hypermethylation of MAPK13 promoter in oesophageal squamous cell carcinoma Is associated with loss of p38δ MAPK expression en
dc.type Article (peer-reviewed) en
dc.internal.authorcontactother Orla P. Barry, Pharmacology & Therapeutics, University College Cork, Cork, Ireland. +353-21-490-3000 Email: o.barry@ucc.ie en
dc.internal.availability Full text available en
dc.date.updated 2015-11-04T10:54:31Z
dc.description.version Published Version en
dc.internal.rssid 323705661
dc.contributor.funder Health Research Board en
dc.description.status Peer reviewed en
dc.identifier.journaltitle Cancers en
dc.internal.copyrightchecked Yes. !!CORA!! Open Access publisher. MPDI titles are open access. DOAJ check and Sherpa Romeo. en
dc.internal.licenseacceptance Yes en
dc.internal.IRISemailaddress o.barry@ucc.ie en


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© 2015 by the authors; licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons by Attribution (CC-BY) license (http://creativecommons.org/licenses/by/4.0/). Except where otherwise noted, this item's license is described as © 2015 by the authors; licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons by Attribution (CC-BY) license (http://creativecommons.org/licenses/by/4.0/).
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