期刊
INTERNATIONAL JOURNAL OF ONCOLOGY
卷 47, 期 3, 页码 1017-1024出版社
SPANDIDOS PUBL LTD
DOI: 10.3892/ijo.2015.3091
关键词
autocrine motility factor; endometrial cancer; epithelial-mesenchymal transition; mesenchymal-epithelial transition; mitogen-activated protein kinase signaling pathway
类别
资金
- National Natural Science Foundation of China [81172476, 81272885, 81472427]
- Science and Technology Commission of Shanghai Municipality [13JC1404501]
- Doctoral Fund of Ministry of Education of China [20120073110090]
Autocrine motility factor (AMF) as a cytokine and a growth factor, is known to regulate tumor cell growth and motility in the progress of various human malignant tumors, however, its role in endometrial cancer (EC) has not been fully studied. In the present study, using immunohistochemistry, we found that AMF was highly expressed in EC tissues compared with normal endometrial tissues and tissue micrio-array technology showed positive correlation between AMF expression and epithelial-to-mesenchymal transition (EMT) related markers E-cadherin, vimentin and Snail. Next, we detected that silencing of AMF by stable transfection with shRNA induced mesenchymal-to-epithelial transition phenotype in Ishikawa and HEC-1B cells by qRT-PCR, western blotting and immunofluorescence. Gene expression profile revealed that AMF silencing resulted in altered expression of EMT related molecular mediators including Snail and transforming growth factor 13 receptor 1, and involvement of mitogen-activated protein kinase (MAPK) signaling pathway. Additionally, we found that EMT related markers were downregulated with pretreatment of the MAPK-specific inhibitor U0126 by western blotting. The present study is the first to support a role for AMF mediating EMT in endometrial cancer through MAPK signaling. Therefore, AMF may provide a potential prognostic and therapeutic target in preventing EC progression.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据