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CXCL11的下调抑制结肠癌细胞的生长和上皮-间质转化。

Down-regulation of CXCL11 inhibits colorectal cancer cell growth and epithelial-mesenchymal transition.

作者信息

Gao Yu Jie, Liu De Lin, Li Sheng, Yuan Gao Feng, Li Li, Zhu Hong Yan, Cao Guan Yi

机构信息

Department of Medical Oncology, Suqian First Hospital, Suqian, Jiangsu, China.

Department of Medical Oncology, Jiangsu Cancer Hospital & Jiangsu Institute of Cancer Research & The Affiliated Cancer Hospital of Nanjing Medical University, Nanjing, Jiangsu, China.

出版信息

Onco Targets Ther. 2018 Oct 23;11:7333-7343. doi: 10.2147/OTT.S167872. eCollection 2018.

DOI:10.2147/OTT.S167872
PMID:30425523
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6205823/
Abstract

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.

摘要

背景

结直肠癌（CRC）预后较差主要是由于局部侵袭和肿瘤转移。上皮-间质转化（EMT）是实体瘤进展的关键步骤，在肿瘤转移中起重要作用。最近的研究表明，C-X-C基序趋化因子11（CXCL11）参与多种癌症的进展。然而，其在结直肠癌中的生物学活性需要更深入的探索。

方法

采用定量实时PCR（qRT-PCR）检测法测定结直肠癌组织和细胞系中CXCL11的水平。分别应用MTT、集落形成、伤口愈合和Transwell侵袭试验评估CXCL11在体外对结直肠癌细胞生长、迁移和侵袭的作用。构建异种移植模型分析CXCL11在体内对结直肠癌细胞生长的功能。

结果

CXCL11在结直肠癌组织和细胞系中过表达。抑制CXCL11可显著抑制体外结直肠癌细胞的迁移、侵袭和EMT。此外，下调CXCL11可降低体内结直肠癌细胞的生长和转移。最后，我们发现抑制CXCL11以N-钙黏蛋白依赖的方式抑制结直肠癌细胞的转移能力。

结论

总之，本研究阐明了CXCL11在结直肠癌细胞生长和转移中的致癌活性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6993/6205823/5cf7cd242d3e/ott-11-7333Fig6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6993/6205823/96d9c6123919/ott-11-7333Fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6993/6205823/a8a82e9f938a/ott-11-7333Fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6993/6205823/db68e06fb3a3/ott-11-7333Fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6993/6205823/6df658110b0e/ott-11-7333Fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6993/6205823/a8c7ba80ebbb/ott-11-7333Fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6993/6205823/5cf7cd242d3e/ott-11-7333Fig6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6993/6205823/96d9c6123919/ott-11-7333Fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6993/6205823/a8a82e9f938a/ott-11-7333Fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6993/6205823/db68e06fb3a3/ott-11-7333Fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6993/6205823/6df658110b0e/ott-11-7333Fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6993/6205823/a8c7ba80ebbb/ott-11-7333Fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6993/6205823/5cf7cd242d3e/ott-11-7333Fig6.jpg

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