دانلود رایگان مقاله انگلیسی جلوگیری ملاتونین از دوباره فعال سازی تکثیر گونه های اکسیژن فعال - هینداوی 2018

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.

5. Conclusion

In summary, melatonin abolishes ROS-promoted growth, metastasis, and angiogenesis in oral cancer. We found that melatonin suppresses ROS production in oral cancer cells. Melatonin inhibits the proliferation and induces the apoptosis of oral cancer cells. Melatonin reduces the migration and invasion of oral cancer cells by the repression of EMT. Moreover, melatonin decreases the angiogenesis of oral cancer. Molecular mechanistically, melatonin exerts antisurvival and antimobility effects by inactivating ROS-dependent Akt signaling and exhibits its antiangiogenesis function by blocking the ROS-activated ERK and Akt pathways in oral cancer. Together, these results indicate that reducing ROS by melatonin probably provides promising therapeutic protection against oral cancer.