Document details

Photonic modulation of EGFR: 280nm low level light arrests cancer cell activation and migration

Author(s): Botelho, C. M. ; Marques, Rogério Filipe Fernandes ; Viruthachalam, Thiagarajan ; Gonçalves, Odete Sofia Lopes ; Vorum, Henrik ; Gomes, Andreia C ; Neves-Petersen, Maria Teresa

Date: 2017

Persistent ID: https://hdl.handle.net/1822/45162

Origin: RepositóriUM - Universidade do Minho

Project/scholarship: info:eu-repo/grantAgreement/EC/H2020/644242/EU; info:eu-repo/grantAgreement/FCT/FARH/SFRH%2FBPD%2F111291%2F2015/PT; info:eu-repo/grantAgreement/FCT/5876/147364/PT; info:eu-repo/grantAgreement/FCT/5876/147337/PT; info:eu-repo/grantAgreement/FCT/5876-PPCDTI/126270/PT ; info:eu-repo/grantAgreement/FCT/COMPETE/126270/PT;

Subject(s): Epidermal growth factor receptor; Activation; Arrest; EGFR; EGF; Cancer cells; Photonic Therapy; Cell Migration; Filopodia; Science & Technology; Ciências Naturais::Ciências Biológicas


Description

Overexpression 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.

The 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).

info:eu-repo/semantics/publishedVersion

Document Type Conference paper
Language English
Contributor(s) Universidade do Minho
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