Melatonin suppresses epithelial-to-mesenchymal transition in the MG-63 cell line

被引:16
|
作者
Chen, Yongjun [1 ]
Zhang, Tao [2 ]
Liu, Xiongwei [1 ]
Li, Zengyan [3 ]
Zhou, Dongming [1 ]
Xu, Wensheng [1 ]
机构
[1] Inner Mongolia Univ Sci & Technol, Affiliated Hosp 1, Dept Orthopaed, Baotou Med Coll, 41 Lin Yin Rd, Baotou 014010, Inner Mongolia, Peoples R China
[2] Inner Mongolia Univ Sci & Technol, Baotou Med Coll, Dept Immunol Basic & Forens Med, Baotou 014060, Inner Mongolia, Peoples R China
[3] Inner Mongolia Univ Sci & Technol, Affiliated Hosp 1, Dept Nephrol, Baotou Med Coll, Baotou 014010, Inner Mongolia, Peoples R China
关键词
MG-63; epithelial-to-mesenchymal transition; melatonin; transforming growth factor beta 1; osteosarcoma; BREAST-CANCER CELLS; CIRCADIAN-RHYTHM; GROWTH; METASTASIS; EXPRESSION; INDUCTION; INVASION; EMT;
D O I
10.3892/mmr.2019.10902
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Epithelial-to-mesenchymal transition (EMT) is a major process involved in tumor progression and metastasis. Melatonin is secreted by the pineal gland and has been documented as a potential therapeutic agent for multiple tumors. However, the effects of melatonin on EMT during osteosarcoma (OA) development remain undefined. The present study explored the biological functions and effects of melatonin on EMT induced by transforming growth factor beta 1 (TGF-beta 1) and its underlying mechanisms in MG-63 cells. Using western-blotting and immunofluorescence, it was found that the switch in E-cadherin/N-cadherin and vimentin expression was induced by TGF-beta 1, which was reversed by melatonin through the suppression of Snail and matrix metalloproteinase 9 (MMP-9), through hypoxia-inducible factor 1 alpha (HIF-1 alpha) inhibition. These findings demonstrated that the anticancer effects of melatonin against OA MG-63 cells is through the suppression of EMT via HIF-1 alpha/Snail/MMP-9 signaling.
引用
收藏
页码:1356 / 1364
页数:9
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