Melatonin attenuates hypoxia-induced epithelial-mesenchymal transition and cell aggressive via Smad7/ CCL20 in glioma
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Xueran Chen1,2, Zhen Wang1,2, Huihui Ma3,4, Shangrong Zhang1,2, Haoran Yang1,2, Hongzhi Wang1,2 and Zhiyou Fang1,2
1Cancer Hospital, Chinese Academy of Sciences, Hefei, Anhui, 230031, China
2Anhui Province Key Laboratory of Medical Physics and Technology, Center of Medical Physics and Technology, Hefei Institutes of Physical Science, Chinese Academy of Sciences, Hefei, Anhui, 230031, China
3Key Laboratory of Ion Beam Bioengineering, Hefei Institutes of Physical Science, Chinese Academy of Sciences, Hefei, Anhui, 230031, China
4Department of Radiation Oncology, First Affiliated Hospital, Anhui Medical University, Hefei, Anhui, 230022, China
Xueran Chen, email: email@example.com
Zhiyou Fang, email: firstname.lastname@example.org
Keywords: melatonin, CCL20, epithelial–mesenchymal transition (EMT), glioma
Received: July 17, 2017 Accepted: August 01, 2017 Published: August 24, 2017
Tumor recurrence in gliomas is partly attributed to increased epithelial–mesenchymal transition (EMT) and enhanced tumor cell dissemination in the adjacent brain parenchyma. Thus, exploring effective strategies for against EMT-like changes in glioma invasion and recurrence will be important for glioma treatment. In this study, we investigated the roles of melatonin in hypoxia-induced EMT suppression, and found that melatonin could significantly suppress the release of the cytokine, CCL20, from cancer cells and antagonize glioma cell metastasis and invasion under hypoxic stress in glioma cells. Furthermore, our findings show that melatonin deregulates Smad7 expression to suppress TGFβ/Smad-mediated increase in CCL20 transcript levels and CCL20-induced EMT occurrence, suggesting a potential anti-EMT therapeutic role for melatonin in malignant transformation in gliomas.
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