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

• Published in: PloS one Vol. 11; no. 9; p. 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: Journal Article
• Language: English
• Published: United States Public Library of Science 15.09.2016; Public Library of Science (PLoS)
• 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; Tumors; Taiwan
• ISSN: 1932-6203; 1932-6203
• DOI: 10.1371/journal.pone.0160586

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.