CCL20 mediates RANK/RANKL-induced epithelial-mesenchymal transition in endometrial cancer cells

被引：33
作者：
Liu, Yao [1 ]
Wang, Jing [1 ]
Ni, Ting [1 ]
Wang, Lihua [1 ]
Wang, Yudong [1 ]
Sun, Xiao [2 ]
机构：
[1] Shanghai Jiao Tong Univ, Int Peace Matern & Child Hlth Hosp, Dept Gynecol, Sch Med, Shanghai 200030, Peoples R China
[2] Shanghai Jiao Tong Univ, Sch Med, Int Peace Matern & Child Hlth Hosp, Lab Gynecol Oncol, Shanghai 200030, Peoples R China
来源：
ONCOTARGET | 2016年 / 7卷 / 18期
基金：
中国国家自然科学基金;
关键词：
CCL20; RANK; RANKL; epithelial-mesenchymal transition; endometrial cancer; LYMPH-NODE METASTASIS; CC-CHEMOKINE RECEPTOR-7; EXPRESSION; MIGRATION; MICROENVIRONMENT; PROLIFERATION; RANK; ACTIVATION; CARCINOMA; INVASION;
D O I：
10.18632/oncotarget.8291
中图分类号：
R73 [肿瘤学];
学科分类号：
100214 ;
摘要：
RANK/RANKL facilitates migration/invasion via epithelial-mesenchymal transition (EMT) in certain malignant tumors. The relationship and mechanism between RANK/RANKL and EMT in endometrial cancer (EC) cells, however, remain unclear. In this study, we firstly showed that RANK/RANKL activation was correlated with EC staging and EMT markers in human EC tissue specimen. RANK/RANKL promoted migration/invasion and initiated EMT of EC cell lines. Then, protein chip analysis and enzyme-linked immunosorbent assay (ELISA) revealed that the expression and secretion of chemokine ligand 20 (CCL20) was dramatically enhanced in RANKL-treated RANK over-expressed EC cells. Moreover, the higher level of CCL20 in both serum and tumor tissue was detected in orthotopic transplantation mouse models. Finally, we confirmed that CCL20 contributed to invasion and EMT of RANK over-expressed EC cells. In summary, all data supported the hypothesis that RANK/RANKL elevated the expression and secretion of CCL20 in EC cells, which promoted cancer progression through EMT.
引用
收藏
页码：25328 / 25339
页数：12
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