FULL ARTICLE Photonic modulation of epidermal growth factor receptor halts receptor activation and cancer cell migration Cláudia M. Botelho 1,2 | Odete Gonçalves 3 | Rogério Marques 2 | Viruthachalam Thiagarajan 4,5 | Henrik Vorum 6 | Andreia C. Gomes 2,3 * | Maria Teresa Neves-Petersen 3,4,6 * 1 Centre of Biological Engineering, Universidade do Minho, Braga, Portugal 2 Centre of Molecular and Environmental Biology (CBMA), Universidade do Minho, Braga, Portugal 3 Department of Health Science and Technology, Aalborg University, Aalborg, Denmark 4 International Iberian Nanotechnology Laboratory (INL), P-4715-310 Braga, Portugal 5 School of Chemistry, Bharathidasan University, Tiruchirappalli, India 6 Department of Clinical Medicine, Aalborg University Hospital, Aalborg, Denmark *Correspondence Andreia Castro Gomes, Centre of Molecular and Environmental Biology (CBMA), Universidade do Minho, 4710-057 Braga, Portugal. Email: agomes@bio.uminho.pt Maria T. Neves-Petersen, International Iberian Nanotechnology Laboratory (INL), P-4715-310 Braga, Portugal. Email: nevespetersen@gmail.com; tneves@dcm. aau.dk Funding information Fundação para a Ciência e a Tecnologia, Grant/ Award Numbers: SFRH/BPD/111291/2015, SFRH/BSAB/ 127924/2016, POCI- 01-0145-FEDER-007569, UID/BIO/04469/2013, COMPETE 2020 (POCI-01-0145-FEDER- 006684), RECI/BBB-EBI/0179/2012 (FCOMP- 01-0124-FEDER-027462) Epidermal growth factor receptor (EGFR) plays a key role in regulating cell survival, proliferation and migration, and its overexpression and activation has been correlated with cancer progression. Cancer therapies targeting EGFR have been applied in the clinic with some success. We show, by confocal microscopy analysis, that illumination of adenocarcinomic human alveolar basal epithelial cells (Human A549—EGFR biosensor cell line) with 280 nm at irradi- ance levels up to 20 times weaker than the Ultraviolet B (UVB) solar output for short periods of time (15-45 minutes) prevents epidermal growth factor-mediated activation of EGFR located on the cell membrane, preventing or reducing cellular disaggregation, formation of filopodia and cell migration. This effect of Ultraviolet (UV) light illumination was confirmed further in a functional scratch assay, and shown to be more effective than that of a specific EGFR-signaling inhibitor. This new photonic approach may be applicable to the treatment of various types of can- cer, alone or in combination with other therapies. KEYWORDS arrest cancer cell migration, EGF, EGFR, metastasis, photonic cancer therapy, protein photochemistry 1 | INTRODUCTION Many current cancer therapies aim at inhibiting the epi- dermal growth factor receptor (EGFR). EGFR is a mem- brane receptor that plays a key role in regulating cell survival and proliferation [1–5], being a member of the ErbB family of receptor tyrosine kinases (RTKs) [6]. EGFR binds to ligands, such as epidermal growth factor (EGF) leading to receptor dimerization and activa- tion of the tyrosine kinase domain [7–9]. This leads to downstream activation of signal transduction cascades, mainly the mitogen-activated protein kinase (MAPK), AKT (or Protein Kinase B) and c-Jun N-terminal kinase (JNK) pathways [10, 11]. These pathways modulate cell migration, adhesion and proliferation. High expression of EGFR is generally associated with cancer progression, invasion, metastasis, late-stage disease, chemotherapy resistance, hormonal therapy resistance and poor general therapeutic outcome [8, 12–15]. Typical che- motherapeutical agents are tyrosine kinase inhibitors that compete with Adenosine triphosphate (ATP) at the intracel- lular tyrosine kinase domain [6, 9, 12] and monoclonal Received: 2 November 2017 Accepted: 12 March 2018 DOI: 10.1002/jbio.201700323 J. Biophotonics. 2018;11:e201700323. www.biophotonics-journal.org © 2018 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim 1 of 12 https://doi.org/10.1002/jbio.201700323