Photonic modulation of epidermal growth factor receptor halts receptor activation and cancer cell migration
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 confoca...
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Published in: | Journal of biophotonics Vol. 11; no. 9; pp. e201700323 - n/a |
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Main Authors: | , , , , , , |
Format: | Journal Article |
Language: | English |
Published: |
Weinheim
Wiley-Blackwell
01-09-2018
WILEY‐VCH Verlag GmbH & Co. KGaA Wiley Subscription Services, Inc |
Subjects: | |
Online Access: | Get full text |
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Summary: | 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 irradiance levels up to 20 times weaker than the UVB solar output for short periods of time (15-45 min) prevents EGF-mediated activation of EGFR located on the cell membrane, preventing or reducing cellular disaggregation, formation of filopodia and cell migration. This effect of 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 cancer, alone or in combination with other therapies.
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) |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 1864-063X 1864-0648 |
DOI: | 10.1002/jbio.201700323 |