Down-regulation of CXCL11 inhibits colorectal cancer cell growth and epithelial-mesenchymal transition.
Down-regulation of CXCL11 inhibits colorectal cancer cell growth and epithelial-mesenchymal transition.
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DOI：
10.2147/ott.s167872
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发表时间：
2018
影响因子：
4
通讯作者：
Cao GY
中科院分区：
文献类型：
--
作者：
Gao YJ;Liu L;Li S;Yuan GF;Li L;Zhu HY;Cao GY
结直肠癌预后差的主要原因是局部侵袭和肿瘤转移。上皮-间充质转化(EMT)是实体瘤发生发展的关键步骤，在肿瘤转移过程中起着至关重要的作用。最近的研究表明，C-X-C基序趋化因子11(CXCL11)参与了多种癌症的发生发展。然而，其在CRC中的生物活性有待于更深层次的探索。采用实时定量聚合酶链式反应(qRT-PCR)检测结直肠癌组织和细胞系中CXCL11的表达水平。采用四甲基偶氮唑盐比色法、集落形成法、伤口愈合实验和Transwell侵袭实验分别检测CXCL11在体外对结直肠癌细胞生长、迁移和侵袭的影响。建立CXCL11异种移植模型，分析CXCL11在结直肠癌细胞体内生长中的作用。CXCL11在结直肠癌组织和细胞系中过表达。抑制CXCL11基因的表达可显著抑制结直肠癌细胞的迁移、侵袭和EMT。此外，CXCL11的下调减少了体内CRC细胞的生长和转移。最后，我们发现CXCL11的抑制以N-钙粘素依赖的方式抑制了CRC细胞的转移能力。综上所述，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。
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. 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. 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. In summary, this study explicates the oncogenic activities of CXCL11 in CRC cell growth and metastasis.