Please use this identifier to cite or link to this item: http://hdl.handle.net/1822/45162

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dc.contributor.authorBotelho, C. M.por
dc.contributor.authorMarques, Rogério Filipe Fernandespor
dc.contributor.authorViruthachalam, Thiagarajanpor
dc.contributor.authorGonçalves, Odete Sofia Lopespor
dc.contributor.authorVorum, Henrikpor
dc.contributor.authorGomes, Andreia C.por
dc.contributor.authorNeves-Petersen, Maria Teresapor
dc.date.accessioned2017-03-24T10:33:39Z-
dc.date.issued2017-02-17-
dc.identifier.isbn9781510605381por
dc.identifier.issn0277-786Xpor
dc.identifier.urihttp://hdl.handle.net/1822/45162-
dc.description.abstractOverexpression of the Epidermal Growth Factor Receptor (EGFR) by cancer cells is associated with a poor prognosis for the patient. For several decades, therapies targeting EGFR have been designed, including the use of monoclonal antibodies and small molecule tyrosine kinase inhibitors. The use of these molecules had good clinical results, although its efficiency (and specificity) is still far from being optimal. In this paper, we present a new approach for a possible new cancer therapy targeting EGFR and using low intensity 280nm light. The influence of 280nm UVB illumination on cancer cells stimulated with 2nM of EGF was followed by time-lapse confocal microscopy. The 280nm illumination of the cancer cells blocks EGFR activation, inhibiting EGFR internalization and cell migration thus inhibiting the transition to the metastatic phenotype. Exposure time is a very important factor. The higher the illumination time the more significant differences were observed: 280nm light delayed or completely halted EGFR activation in the cell membrane, mainly at the cell junction level, and delayed or halted EGFR endocytic internalization, filopodia formation and cell migration.por
dc.description.sponsorshipThe authors acknowledge the funding from the European Commission through the project H2020-644242 – SAPHELY and the project H2020-634013-2-PHOCNOSIS. The authors also acknowledge the Portuguese Foundation for Science and Technology (FCT) for the grant SFRH/BPD/111291/2015. This work was supported by the strategic programme UID/BIA/04050/2013 (POCI-01-0145-FEDER-007569) funded by national funds through the FCT I.P. and by the ERDF through the COMPETE2020 - Programa Operacional Competitividade e Internacionalização (POCI). This work was also supported by FCT under the scope of the strategic funding of UID/BIO/04469/2013 unit and COMPETE 2020 (POCI-01-0145-FEDER-006684) and the Project RECI/BBB-EBI/0179/2012 (FCOMP-01-0124FEDER-027462).por
dc.language.isoengpor
dc.publisherSociety of Photo-optical Instrumentation Engineerspor
dc.relationinfo:eu-repo/grantAgreement/EC/H2020/644242/EU-
dc.relationSFRH/BPD/111291/2015-
dc.relationinfo:eu-repo/grantAgreement/FCT/5876/147364/PT-
dc.relationinfo:eu-repo/grantAgreement/FCT/5876/147337/PT-
dc.relationinfo:eu-repo/grantAgreement/FCT/5876-PPCDTI/126270/PT-
dc.relationinfo:eu-repo/grantAgreement/FCT/COMPETE/126270/PT-
dc.rightsrestrictedAccesspor
dc.subjectEpidermal growth factor receptorpor
dc.subjectActivationpor
dc.subjectArrestpor
dc.subjectEGFRpor
dc.subjectEGFpor
dc.subjectCancer cellspor
dc.subjectPhotonic Therapypor
dc.subjectCell Migrationpor
dc.subjectFilopodiapor
dc.titlePhotonic modulation of EGFR: 280nm low level light arrests cancer cell activation and migrationpor
dc.typeconferencePaperpor
dc.peerreviewedyespor
oaire.citationStartPage1por
oaire.citationEndPage8por
oaire.citationTitleMechanisms of Photobiomodulation Therapy XIIpor
oaire.citationVolume10048por
dc.identifier.doi10.1117/12.2249038por
dc.subject.fosCiências Naturais::Ciências Biológicaspor
dc.description.publicationversioninfo:eu-repo/semantics/publishedVersionpor
dc.subject.wosScience & Technologypor
sdum.journalProceedings of SPIEpor
sdum.conferencePublicationMechanisms of Photobiomodulation Therapy XIIpor
Appears in Collections:CEB - Artigos em Livros de Atas / Papers in Proceedings
DBio - Comunicações/Communications in Congresses

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