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Article: Interactions between E-cadherin and microRNA deregulation in head and neck cancers: The potential interplay

TitleInteractions between E-cadherin and microRNA deregulation in head and neck cancers: The potential interplay
Authors
Issue Date2014
PublisherHindawi Publishing Corporation. The Journal's web site is located at http://www.hindawi.com/journals/jbb/index.html
Citation
Biomed Research International, 2014, v. 2014, article no. 126038 How to Cite?
AbstractE-cadherin expression in the head and neck epithelium is essential for the morphogenesis and homeostasis of epithelial tissues. The cadherin-mediated cell-cell contacts are required for the anchorage-dependent growth of epithelial cells. Further, survival and proliferation require physical tethering created by proper cell-cell adhesion. Otherwise, the squamous epithelial cells will undergo programmed cell death. Head and neck cancers can escape from anoikis and enter into the epithelial-mesenchymal transition stages via the modulation of E-cadherin expression with epigenetic mechanisms. At epigenetic level, gene expression control is not dependent on the DNA sequence. In the context of E-cadherin regulation in head and neck cancers, 2 major mechanisms including de novo promoter hypermethylation and microRNA dysregulation are most extensively studied. Both of them control E-cadherin expression at transcription level and subsequently hinder the overall E-cadherin protein level in the head and neck cancer cells. Increasing evidence suggested that microRNA mediated E-cadherin expression in the head and neck cancers by directly/indirectly targeting the transcription suppressors of E-cadherin, ZEB1 and ZEB2.
Persistent Identifierhttp://hdl.handle.net/10722/200939
ISSN
2015 Impact Factor: 2.134
2015 SCImago Journal Rankings: 0.725
PubMed Central ID

 

DC FieldValueLanguage
dc.contributor.authorWong, TSen_US
dc.contributor.authorGao, Wen_US
dc.contributor.authorChan, JYWen_US
dc.date.accessioned2014-08-21T07:07:39Z-
dc.date.available2014-08-21T07:07:39Z-
dc.date.issued2014en_US
dc.identifier.citationBiomed Research International, 2014, v. 2014, article no. 126038en_US
dc.identifier.issn2314-6133-
dc.identifier.urihttp://hdl.handle.net/10722/200939-
dc.description.abstractE-cadherin expression in the head and neck epithelium is essential for the morphogenesis and homeostasis of epithelial tissues. The cadherin-mediated cell-cell contacts are required for the anchorage-dependent growth of epithelial cells. Further, survival and proliferation require physical tethering created by proper cell-cell adhesion. Otherwise, the squamous epithelial cells will undergo programmed cell death. Head and neck cancers can escape from anoikis and enter into the epithelial-mesenchymal transition stages via the modulation of E-cadherin expression with epigenetic mechanisms. At epigenetic level, gene expression control is not dependent on the DNA sequence. In the context of E-cadherin regulation in head and neck cancers, 2 major mechanisms including de novo promoter hypermethylation and microRNA dysregulation are most extensively studied. Both of them control E-cadherin expression at transcription level and subsequently hinder the overall E-cadherin protein level in the head and neck cancer cells. Increasing evidence suggested that microRNA mediated E-cadherin expression in the head and neck cancers by directly/indirectly targeting the transcription suppressors of E-cadherin, ZEB1 and ZEB2.-
dc.languageengen_US
dc.publisherHindawi Publishing Corporation. The Journal's web site is located at http://www.hindawi.com/journals/jbb/index.html-
dc.relation.ispartofBiomed Research Internationalen_US
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.titleInteractions between E-cadherin and microRNA deregulation in head and neck cancers: The potential interplayen_US
dc.typeArticleen_US
dc.identifier.emailWong, TS: thiansze@graduate.hku.hken_US
dc.identifier.emailGao, W: weigao@graduate.hku.hken_US
dc.identifier.emailChan, JYW: jywchan1@hku.hken_US
dc.identifier.authorityChan, JYW=rp01314en_US
dc.identifier.authorityWong, TS=rp00478en_US
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.1155/2014/126038-
dc.identifier.pmid25161999-
dc.identifier.pmcidPMC4138976-
dc.identifier.scopuseid_2-s2.0-84929939903-
dc.identifier.hkuros233202en_US
dc.identifier.volume2014en_US
dc.publisher.placeUnited States-

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