Down-regulation of CXCL 11 inhibits colorectal cancer cell growth and epithelial-mesenchymal transition
Authors Gao YJ, Liu DL, Li S, Yuan GF, Li L, Zhu HY, Cao GY
Received 11 March 2018
Accepted for publication 22 July 2018
Published 23 October 2018 Volume 2018:11 Pages 7333—7343
Checked for plagiarism Yes
Review by Single-blind
Peer reviewers approved by Dr Colin Mak
Peer reviewer comments 2
Editor who approved publication: Professor Jianmin Xu
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
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