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dc.contributor.authorPitta, Chara A.en
dc.contributor.authorPapageorgis, P.en
dc.contributor.authorCharalambous, Christinaen
dc.contributor.authorConstantinou, Andreas I.en
dc.creatorPitta, Chara A.en
dc.creatorPapageorgis, P.en
dc.creatorCharalambous, Christinaen
dc.creatorConstantinou, Andreas I.en
dc.date.accessioned2019-11-04T12:52:31Z
dc.date.available2019-11-04T12:52:31Z
dc.date.issued2013
dc.identifier.urihttp://gnosis.library.ucy.ac.cy/handle/7/53319
dc.description.abstractThe purpose of this work is to determine the molecular mechanisms underlying tamoxifen resistance. We show here that ER-β is epigenetically silenced in a cell line with acquired tamoxifen resistance (MCF-7/TAM-R) and this could be reversed by 5-AZA-deoxycytidine (5-AZA) and trichostatin-A (TSA) pre-treatment. Subsequent treatment with 4-hydroxy-tamoxifen (4-OHT) induced ER-β nuclear translocation, upregulated pS2 and p21 levels and reduced cell viability. Transfection with an ER-β expression vector sensitized MCF-7/TAM-R cells to the growth inhibitory and pro-apoptotic effects of 4-OHT, indicating that ER-β re-expression alone is sufficient to restore sensitivity to tamoxifen. This novel finding reveals that ER-β is fundamental in overcoming acquired tamoxifen resistance and provides insights for new therapeutic protocols against breast cancer. © 2013 Elsevier Ireland Ltd.en
dc.sourceCancer lettersen
dc.source.urihttps://www.scopus.com/inward/record.uri?eid=2-s2.0-84880509091&doi=10.1016%2fj.canlet.2013.05.031&partnerID=40&md5=039242b9514d8cb1cf6a32040cf52868
dc.subject17β estradiolel
dc.subjectER-αel
dc.subjectER-βel
dc.subjectestrogen receptor αel
dc.subjectestrogen receptor βel
dc.subjectarticleen
dc.subjectFemaleen
dc.subjectHumansen
dc.subjectBreast Neoplasmsen
dc.subjectcontrolled studyen
dc.subjectpriority journalen
dc.subjectTime Factorsen
dc.subjectprotein expressionen
dc.subjectBreast canceren
dc.subjectapoptosisen
dc.subjectestrogen receptor betaen
dc.subjectTamoxifenen
dc.subjectcancer resistanceen
dc.subjectprotein p21en
dc.subjectprotein pS2en
dc.subjectchemosensitivityen
dc.subjectcell strain MCF 7en
dc.subjectMCF-7 Cellsen
dc.subjectCell Survivalen
dc.subjectcell viabilityen
dc.subjectcell cycle arresten
dc.subjectTransfectionen
dc.subjectDose-Response Relationship, Drugen
dc.subjectAntineoplastic Agents, Hormonalen
dc.subjectprotein transporten
dc.subjecthistone deacetylaseen
dc.subjectGene Expression Regulation, Neoplasticen
dc.subjectChromatin Assembly and Disassemblyen
dc.subjectEpigeneticsen
dc.subjectDNMTen
dc.subjectHDACen
dc.subject3-(4,5-dimethylthiazol-2-yl)-2,5-monotetrazolium bromideen
dc.subject4-hydroxytamoxifenen
dc.subject4-OHTen
dc.subject5 aza 2' deoxycytidineen
dc.subject5-2′-deoxycytidineen
dc.subject5-AZAen
dc.subjectActive Transport, Cell Nucleusen
dc.subjectAzacitidineen
dc.subjectDNA methyl transferasesen
dc.subjectDrug Resistance, Neoplasmen
dc.subjectE(2)en
dc.subjectE2en
dc.subjectEstrogen receptorsen
dc.subjectexpression vectoren
dc.subjectGene Silencingen
dc.subjectHistone Deacetylase Inhibitorsen
dc.subjectHydroxamic Acidsen
dc.subjecthydroxytamoxifenen
dc.subjectMTTen
dc.subjectselective estrogen receptor modulatorsen
dc.subjectSERMsen
dc.subjectTamoxifen resistanceen
dc.subjecttrichostatin Aen
dc.subjectTSAen
dc.titleReversal of ER-β silencing by chromatin modifying agents overrides acquired tamoxifen resistanceen
dc.typeinfo:eu-repo/semantics/article
dc.identifier.doi10.1016/j.canlet.2013.05.031
dc.description.volume337
dc.description.startingpage167
dc.description.endingpage176
dc.author.facultyΣχολή Θετικών και Εφαρμοσμένων Επιστημών / Faculty of Pure and Applied Sciences
dc.author.departmentΤμήμα Βιολογικών Επιστημών / Department of Biological Sciences
dc.type.uhtypeArticleen
dc.description.notes<p>Manufacturers: Alexis, Switzerlanden
dc.description.notesCited By :9</p>en
dc.source.abbreviationCancer Lett.en
dc.contributor.orcidConstantinou, Andreas I. [0000-0003-0365-1821]
dc.gnosis.orcid0000-0003-0365-1821


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