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Oxidative Medicine and Cellular Longevity
Volume 2018 (2018), Article ID 3510970, 13 pages
https://doi.org/10.1155/2018/3510970
Research Article

Melatonin Inhibits Reactive Oxygen Species-Driven Proliferation, Epithelial-Mesenchymal Transition, and Vasculogenic Mimicry in Oral Cancer

1Department of Stomatology, Daping Hospital and Research Institute of Surgery, Third Military Medical University, Chongqing 400042, China
2School and Hospital of Stomatology, Wenzhou Medical University, Wenzhou, Zhejiang 325035, China
3Department of Infection and Immunity, State Key Laboratory of Trauma, Burn and Combined Injury, Daping Hospital and Research Institute of Surgery, Third Military Medical University, Chongqing 400042, China
4Department of Nursing, Xi’an International University, Xi’an 710077, China
5State Key Laboratory of Military Stomatology and National Clinical Research Center for Oral Diseases, Department of Periodontology, School of Stomatology, Fourth Military Medical University, Xi’an 710032, China
6Department of Maxillofacial Surgery, Daping Hospital and Research Institute of Surgery, Third Military Medical University, Chongqing 400042, China
7Department of Stomatology, 8th Hospital of People’s Liberation Army, Shigatse 857000, China

Correspondence should be addressed to Lei Li; moc.amuartjc@iliel and Xin Nie; moc.361@piveinnix

Received 30 October 2017; Revised 9 January 2018; Accepted 23 January 2018; Published 21 March 2018

Academic Editor: Aramati B. M. Reddy

Copyright © 2018 Rui Liu et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Globally, oral cancer is the most common type of head and neck cancers. Melatonin elicits inhibitory effects on oral cancer; however, the biological function of melatonin and underlying mechanisms remain largely unknown. In this study, we found that melatonin impaired the proliferation and apoptosis resistance of oral cancer cells by inactivating ROS-dependent Akt signaling, involving in downregulation of cyclin D1, PCNA, and Bcl-2 and upregulation of Bax. Melatonin inhibited the migration and invasion of oral cancer cells by repressing ROS-activated Akt signaling, implicating with the reduction of Snail and Vimentin and the enhancement of E-cadherin. Moreover, melatonin hampered vasculogenic mimicry of oral cancer cells through blockage of ROS-activated extracellular-regulated protein kinases (ERKs) and Akt pathways involving the hypoxia-inducible factor 1α. Consistently, melatonin retarded tumorigenesis of oral cancer in vivo. Overall, these findings indicated that melatonin exerts antisurvival, antimotility, and antiangiogenesis effects on oral cancer partly by suppressing ROS-reliant Akt or ERK signaling.