| Summary: | 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
|
|---|
