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

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

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 corr...

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Main Authors: Liu, Yao, Wang, Jing, Ni, Ting, Wang, Lihua, Wang, Yudong, Sun, Xiao
Format: Online
Language:English
Published: Impact Journals LLC 2016
Online Access:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5041907/
id pubmed-5041907
recordtype oai_dc
spelling pubmed-50419072016-10-10 CCL20 mediates RANK/RANKL-induced epithelial-mesenchymal transition in endometrial cancer cells Liu, Yao Wang, Jing Ni, Ting Wang, Lihua Wang, Yudong Sun, Xiao Research Paper 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. Impact Journals LLC 2016-03-23 /pmc/articles/PMC5041907/ /pubmed/27015366 http://dx.doi.org/10.18632/oncotarget.8291 Text en Copyright: © 2016 Liu et al. http://creativecommons.org/licenses/by/2.5/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
repository_type Open Access Journal
institution_category Foreign Institution
institution US National Center for Biotechnology Information
building NCBI PubMed
collection Online Access
language English
format Online
author Liu, Yao
Wang, Jing
Ni, Ting
Wang, Lihua
Wang, Yudong
Sun, Xiao
spellingShingle Liu, Yao
Wang, Jing
Ni, Ting
Wang, Lihua
Wang, Yudong
Sun, Xiao
CCL20 mediates RANK/RANKL-induced epithelial-mesenchymal transition in endometrial cancer cells
author_facet Liu, Yao
Wang, Jing
Ni, Ting
Wang, Lihua
Wang, Yudong
Sun, Xiao
author_sort Liu, Yao
title CCL20 mediates RANK/RANKL-induced epithelial-mesenchymal transition in endometrial cancer cells
title_short CCL20 mediates RANK/RANKL-induced epithelial-mesenchymal transition in endometrial cancer cells
title_full CCL20 mediates RANK/RANKL-induced epithelial-mesenchymal transition in endometrial cancer cells
title_fullStr CCL20 mediates RANK/RANKL-induced epithelial-mesenchymal transition in endometrial cancer cells
title_full_unstemmed CCL20 mediates RANK/RANKL-induced epithelial-mesenchymal transition in endometrial cancer cells
title_sort ccl20 mediates rank/rankl-induced epithelial-mesenchymal transition in endometrial cancer cells
description 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.
publisher Impact Journals LLC
publishDate 2016
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5041907/
_version_ 1613665561763381248

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