Loss of p38δ mitogen-activated protein kinase expression promotes oesophageal squamous cell carcinoma proliferation, migration and anchorage-independent growth.

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dc.contributor.author O'Callaghan, Carol
dc.contributor.author Fanning, Liam J.
dc.contributor.author Houston, Aileen M.
dc.contributor.author Barry, Orla P.
dc.date.accessioned 2016-06-17T14:51:15Z
dc.date.available 2016-06-17T14:51:15Z
dc.date.issued 2013-05-29
dc.identifier.citation O'Callaghan C., Fanning L., Houston A and Barry OPB. (2013) 'Loss of p38 delta mitogen-activated protein kinase expression promotes oesophageal squamous cell carcinoma proliferation, migration and anchorage-independent growth', International Journal of Oncology, 43, pp. 405-415. http://dx.doi.org/10.3892/ijo.2013.1968 en
dc.identifier.volume 43 en
dc.identifier.startpage 405 en
dc.identifier.endpage 415 en
dc.identifier.issn 1019-6439
dc.identifier.issn 1791-2423
dc.identifier.uri http://hdl.handle.net/10468/2757
dc.identifier.doi 10.3892/ijo.2013.1968
dc.description.abstract Oesophageal cancer is an aggressive tumour which responds poorly to both chemotherapy and radiation therapy and has a poor prognosis. Thus, a greater understanding of the biology of oesophageal cancer is needed in order to identify novel therapeutic targets. Among these targets p38 MAPK isoforms are becoming increasingly important for a variety of cellular functions. The physiological functions of p38α and -β are now well documented in contrast to -γ and -δ which are comparatively under-studied and ill-defined. A major obstacle to deciphering the role(s) of the latter two p38 isoforms is the lack of specific chemical activators and inhibitors. In this study, we analysed p38 MAPK isoform expression in oesophageal cancer cell lines as well as human normal and tumour tissue. We observed specifically differential p38δ expression. The role(s) of p38δ and active (phosphorylated) p38δ (p-p38δ) in oesophageal squamous cell carcinoma (OESCC) was delineated using wild-type p38δ as well as active p-p38δ, generated by fusing p38δ to its upstream activator MKK6b(E) via a decapeptide (Gly-Glu)5 linker. OESCC cell lines which are p38δ-negative (KE-3 and -8) grew more quickly than cell lines (KE-6 and -10) which express endogenous p38δ. Re-introduction of p38δ resulted in a time-dependent decrease in OESCC cell proliferation which was exacerbated with p-p38δ. In addition, we observed that p38δ and p-p38δ negatively regulated OESCC cell migration in vitro. Finally both p38δ and p-p38δ altered OESCC anchorage-independent growth. Our results suggest that p38δ and p-p38δ have a role in the suppression of OESCC. Our research may provide a new potential target for the treatment of oesophageal cancer. en
dc.description.sponsorship Health Research Board (grant HRA/2009/17). en
dc.format.mimetype application/pdf en
dc.language.iso en en
dc.publisher Spandidos Publications en
dc.rights © O'Callaghan et al. This is an open access article distributed under the terms of Creative Commons Attribution License [CC BY_NC 3.0]. en
dc.rights.uri https://creativecommons.org/licenses/by-nc/3.0/ en
dc.subject Oesophageal cancer en
dc.subject p38 MAPK isoforms en
dc.subject Oesophageal squamous cell carcinoma en
dc.subject Cell migration en
dc.subject Cell proliferation en
dc.subject RNA en
dc.subject p38δ mitogen-activated protein kinase en
dc.subject Anchorage-independent growth en
dc.title Loss of p38δ mitogen-activated protein kinase expression promotes oesophageal squamous cell carcinoma proliferation, migration and anchorage-independent growth. en
dc.type Article (peer-reviewed) en
dc.internal.authorcontactother Liam J. Fanning, Medicine Department, University College Cork, Cork, Ireland. +353-21-490-3000 Email: l.fanning@ucc.ie en
dc.internal.authorcontactother Aileen Houston, Medicine Department , University College Cork, Cork, Ireland. +353-21-490-3000 Email: a.houston@ucc.ie en
dc.internal.availability Full text available en
dc.date.updated 2013-05-30T15:05:33Z
dc.description.version Published Version en
dc.internal.rssid 211150221
dc.internal.rssid 215100482
dc.contributor.funder Health Research Board en
dc.description.status Peer reviewed en
dc.identifier.journaltitle International Journal of Oncology en
dc.internal.copyrightchecked No !!CORA!! en
dc.internal.licenseacceptance Yes en
dc.internal.IRISemailaddress l.fanning@ucc.ie en
dc.internal.IRISemailaddress a.houston@ucc.ie en


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© O'Callaghan et al. This is an open access article distributed under the terms of Creative Commons Attribution License [CC BY_NC 3.0]. Except where otherwise noted, this item's license is described as © O'Callaghan et al. This is an open access article distributed under the terms of Creative Commons Attribution License [CC BY_NC 3.0].
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