The regulation of Toll-like receptor 2 by miR-143 suppresses the invasion and migration of a subset of human colorectal carcinoma cells.

The regulation of Toll-like receptor 2 by miR-143 suppresses the invasion and migration of a subset of human colorectal carcinoma cells.
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miR-143对Toll样受体2的调节抑制人结直肠癌细胞亚群的侵袭和迁移

DOI:
10.1186/1476-4598-12-77
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发表时间:
2013-07-17
期刊:
影响因子:
37.3
通讯作者:
Zhang J
Zhang J
中科院分区:
医学1区
文献类型:
--
作者:
Guo H;Chen Y;Hu X;Qian G;Ge S;Zhang J

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BackgroundThe Toll样受体2(TLR 2)驱动的组织反应可能促进新血管生成和肿瘤生长的机制知之甚少。MethodsWe研究了TLR 2和相关的miRNA在结直肠癌(CRC)组织和细胞系中的表达水平,采用实时PCR,北方印迹和Western印迹。生存曲线生成的对数秩检验和TLR 2信号在肿瘤的侵袭和迁移的作用,确定transwell分析kitchs.ResultsWe观察到,从CRC患者的组织表达相对较高水平的TLR 2。靶向TLR 2显著降低CRC细胞的侵袭和迁移。我们还发现,miR-143是一种在CRC组织中下调的假定肿瘤抑制因子,主要通过TLR 2减少CRC细胞的侵袭和迁移。利用异种移植小鼠模型,我们证明,重新表达的miR-143抑制CRC细胞在vivo.ConclusionmiR-143块TLR 2信号通路在人类CRC细胞的殖民。这些知识可能为利用miR-143模拟物治疗CRC患者的新临床应用铺平道路。
BackgroundThe Toll-like receptor 2 (TLR2)-driven tissue response may promote neoangiogenesis and tumour growth by mechanisms that are poorly understood.MethodsWe investigated the expression levels of TLR2 and associated-miRNAs in colorectal carcinoma (CRC) tissues and cell lines using real-time PCR, northern blotting and western blotting. Survival curver was generated by Log-Rank test and the role of TLR2 signalling in tumour invasion and migration was determined by transwell analysis kits.ResultsWe observed that the tissues from CRC patients express relatively high levels of TLR2. Targeting TLR2 markedly reduces the invasion and migration of CRC cells. We also found that miR-143, a putative tumour suppressor that is down-regulated in CRC tissues, reduces the invasion and migration of CRC cells primarily via TLR2. Utilising a xenograft mouse model, we demonstrated that re-expression of miR-143 inhibits CRC cell colonisation in vivo.ConclusionmiR-143 blocks the TLR2 signalling pathway in human CRC cells. This knowledge may pave the way for new clinical applications utilising miR-143 mimics in the treatment of patients with CRC.
DOI: 10.1128/iai.68.12.7010-7017.2000
发表时间: 2000-12-01
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