Down-regulation of CXCL 11 inhibits colorectal cancer cell growth and epithelial-mesenchymal transition

Yu Jie Gao,1 De Lin Liu,2 Sheng Li,2 Gao Feng Yuan,1 Li Li,1 Hong Yan Zhu,3 Guan Yi Cao3 1Department of Medical Oncology, Suqian First Hospital, Suqian, Jiangsu, China; 2Department of Medical Oncology, Jiangsu Cancer Hospital & Jiangsu Institute of Cancer Research & The Affiliated C...

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Main Authors: Gao YJ, Liu DL, Li S, Yuan GF, Li L, Zhu HY, Cao GY
Format: Article
Language:English
Published: Dove Medical Press 2018-10-01
Series:OncoTargets and Therapy
Subjects:
CRC
EMT
Online Access:https://www.dovepress.com/down-regulation-of-cxcl-11-inhibits-colorectal-cancer-cell-growth-and--peer-reviewed-article-OTT
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spelling doaj-7f1ed2a010b24f9d9b418611a0d02d712020-11-24T21:48:26ZengDove Medical PressOncoTargets and Therapy1178-69302018-10-01Volume 117333734341649Down-regulation of CXCL 11 inhibits colorectal cancer cell growth and epithelial-mesenchymal transitionGao YJLiu DLLi SYuan GFLi LZhu HYCao GYYu Jie Gao,1 De Lin Liu,2 Sheng Li,2 Gao Feng Yuan,1 Li Li,1 Hong Yan Zhu,3 Guan Yi Cao3 1Department of Medical Oncology, Suqian First Hospital, Suqian, Jiangsu, China; 2Department of Medical Oncology, Jiangsu Cancer Hospital & Jiangsu Institute of Cancer Research & The Affiliated Cancer Hospital of Nanjing Medical University, Nanjing, Jiangsu, China; 3Department of General Surgery, Suqian First Hospital, Suqian, Jiangsu, China Background: The poor prognosis of colorectal cancer (CRC) largely results from local invasion and tumor metastases. Epithelial-mesenchymal transition (EMT) is a key step in the progression of solid tumors and plays a vital role in tumor metastasis. Recent studies demonstrate that C-X-C motif chemokine 11 (CXCL11) is involved in various cancers’ progression. However, its biological activity in CRC needs deeper exploration. Methods: The level of CXCL11 in CRC tissues and cell lines was determined using the quantitative real-time PCR (qRT-PCR) assay. The MTT, colony formation, wound healing and Transwell invasion assays were applied to assess the role of CXCL11 in CRC cell growth, migration and invasion, in vitro, respectively. A xenograft model was constructed to analyze the function of CXCL11 in CRC cell growth in vivo. Results: CXCL11 was over-expressed in CRC tissues and cell lines. Repression of CXCL11 significantly inhibited CRC cell migration, invasion and EMT in vitro. In addition, down-regulation of CXCL11 reduced CRC cell growth and metastasis in vivo. Finally, we revealed that repression of CXCL11 inhibited the metastatic ability of CRC cell in a N-cadherin dependent manner. Conclusion: In summary, this study explicates the oncogenic activities of CXCL11 in CRC cell growth and metastasis. Keywords: colon cancer, CXCL11, migration, invasion, EMThttps://www.dovepress.com/down-regulation-of-cxcl-11-inhibits-colorectal-cancer-cell-growth-and--peer-reviewed-article-OTTCRCCXCL11MetastasisEMT
collection DOAJ
language English
format Article
sources DOAJ
author Gao YJ
Liu DL
Li S
Yuan GF
Li L
Zhu HY
Cao GY
spellingShingle Gao YJ
Liu DL
Li S
Yuan GF
Li L
Zhu HY
Cao GY
Down-regulation of CXCL 11 inhibits colorectal cancer cell growth and epithelial-mesenchymal transition
OncoTargets and Therapy
CRC
CXCL11
Metastasis
EMT
author_facet Gao YJ
Liu DL
Li S
Yuan GF
Li L
Zhu HY
Cao GY
author_sort Gao YJ
title Down-regulation of CXCL 11 inhibits colorectal cancer cell growth and epithelial-mesenchymal transition
title_short Down-regulation of CXCL 11 inhibits colorectal cancer cell growth and epithelial-mesenchymal transition
title_full Down-regulation of CXCL 11 inhibits colorectal cancer cell growth and epithelial-mesenchymal transition
title_fullStr Down-regulation of CXCL 11 inhibits colorectal cancer cell growth and epithelial-mesenchymal transition
title_full_unstemmed Down-regulation of CXCL 11 inhibits colorectal cancer cell growth and epithelial-mesenchymal transition
title_sort down-regulation of cxcl 11 inhibits colorectal cancer cell growth and epithelial-mesenchymal transition
publisher Dove Medical Press
series OncoTargets and Therapy
issn 1178-6930
publishDate 2018-10-01
description Yu Jie Gao,1 De Lin Liu,2 Sheng Li,2 Gao Feng Yuan,1 Li Li,1 Hong Yan Zhu,3 Guan Yi Cao3 1Department of Medical Oncology, Suqian First Hospital, Suqian, Jiangsu, China; 2Department of Medical Oncology, Jiangsu Cancer Hospital & Jiangsu Institute of Cancer Research & The Affiliated Cancer Hospital of Nanjing Medical University, Nanjing, Jiangsu, China; 3Department of General Surgery, Suqian First Hospital, Suqian, Jiangsu, China Background: The poor prognosis of colorectal cancer (CRC) largely results from local invasion and tumor metastases. Epithelial-mesenchymal transition (EMT) is a key step in the progression of solid tumors and plays a vital role in tumor metastasis. Recent studies demonstrate that C-X-C motif chemokine 11 (CXCL11) is involved in various cancers’ progression. However, its biological activity in CRC needs deeper exploration. Methods: The level of CXCL11 in CRC tissues and cell lines was determined using the quantitative real-time PCR (qRT-PCR) assay. The MTT, colony formation, wound healing and Transwell invasion assays were applied to assess the role of CXCL11 in CRC cell growth, migration and invasion, in vitro, respectively. A xenograft model was constructed to analyze the function of CXCL11 in CRC cell growth in vivo. Results: CXCL11 was over-expressed in CRC tissues and cell lines. Repression of CXCL11 significantly inhibited CRC cell migration, invasion and EMT in vitro. In addition, down-regulation of CXCL11 reduced CRC cell growth and metastasis in vivo. Finally, we revealed that repression of CXCL11 inhibited the metastatic ability of CRC cell in a N-cadherin dependent manner. Conclusion: In summary, this study explicates the oncogenic activities of CXCL11 in CRC cell growth and metastasis. Keywords: colon cancer, CXCL11, migration, invasion, EMT
topic CRC
CXCL11
Metastasis
EMT
url https://www.dovepress.com/down-regulation-of-cxcl-11-inhibits-colorectal-cancer-cell-growth-and--peer-reviewed-article-OTT
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