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2018 ; 2018
(ä): 3510970
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Melatonin Inhibits Reactive Oxygen Species-Driven Proliferation,
Epithelial-Mesenchymal Transition, and Vasculogenic Mimicry in Oral Cancer
#MMPMID29725496
Liu R
; Wang HL
; Deng MJ
; Wen XJ
; Mo YY
; Chen FM
; Zou CL
; Duan WF
; Li L
; Nie X
Oxid Med Cell Longev
2018[]; 2018
(ä): 3510970
PMID29725496
show ga
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 1?. 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.