RelA-Mediated BECN1 Expression Is Required for Reactive Oxygen Species-Induced Autophagy in Oral Cancer Cells Exposed to Low-Power Laser Irradiation

Low-power laser irradiation (LPLI) is a non-invasive and safe method for cancer treatment that alters a variety of physiological processes in the cells. Autophagy can play either a cytoprotective role or a detrimental role in cancer cells exposed to stress. The detailed mechanisms of autophagy and i...

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Published in:PloS one 2016-09, Vol.11 (9), p.e0160586-e0160586
Main Authors: Shu, Chih-Wen, Chang, Hong-Tai, Wu, Chieh-Shan, Chen, Chien-Hsun, Wu, Sam, Chang, Hsueh-Wei, Kuo, Soong-Yu, Fu, Earl, Liu, Pei-Feng, Hsieh, Yao-Dung
Format: Article
Language:English
Subjects:
Apoptosis
Autophagy
Beclin-1 - metabolism
Biology and Life Sciences
Cancer
Cancer cells
Cancer therapies
Cancer treatment
Cell cycle
Cell death
Cytotoxicity
Engineering and Technology
Exposure
Flux density
Gene expression
Health education
Humans
Irradiation
Kinases
Lasers
Low-Level Light Therapy
Medicine and Health Sciences
Metabolism
Mouth cancer
Mouth Neoplasms - immunology
Mouth Neoplasms - pathology
NF-kappa B - metabolism
Oral cancer
Oxygen
Phagocytosis
Pharmacology
Reactive oxygen species
Reactive Oxygen Species - metabolism
RelA protein
Research and Analysis Methods
Toxicity
Transcription
Transcription Factor RelA - metabolism
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Summary:Low-power laser irradiation (LPLI) is a non-invasive and safe method for cancer treatment that alters a variety of physiological processes in the cells. Autophagy can play either a cytoprotective role or a detrimental role in cancer cells exposed to stress. The detailed mechanisms of autophagy and its role on cytotoxicity in oral cancer cells exposed to LPLI remain unclear. In this study, we showed that LPLI at 810 nm with energy density 60 J/cm2 increased the number of microtubule associated protein 1 light chain 3 (MAP1LC3) puncta and increased autophagic flux in oral cancer cells. Moreover, reactive oxygen species (ROS) production was induced, which increased RelA transcriptional activity and beclin 1 (BECN1) expression in oral cancer cells irradiated with LPLI. Furthermore, ROS scavenger or knockdown of RelA diminished LPLI-induced BECN1 expression and MAP1LC3-II conversion. In addition, pharmacological and genetic ablation of autophagy significantly enhanced the effects of LPLI-induced apoptosis in oral cancer cells. These results suggest that autophagy may be a resistant mechanism for LPLI-induced apoptosis in oral cancer cells.
ISSN:1932-6203
1932-6203
DOI:10.1371/journal.pone.0160586