LncRNA CRNDE triggers inflammation through the TLR3-NF-B-Cytokine signaling pathway
LncRNA CRNDE triggers inflammation through the TLR3-NF-B-Cytokine signaling pathway
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LncRNA CRNDE 通过 TLR3-NF-B-细胞因子信号通路触发炎症
DOI：
10.1177/1010428317703821
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发表时间：
2017-06-16
期刊：
影响因子：
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通讯作者：
Wang, Yajie
中科院分区：
文献类型：
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作者：
Li, Haowen;Li, Qi;Wang, Yajie
大肠肿瘤差异表达基因（CRNDE）是一种在多种肿瘤细胞中高表达的癌基因，影响细胞增殖、迁移、侵袭和凋亡。其功能和作用机制是目前研究的热点。本研究利用基因芯片技术分析CRNDE过表达细胞中的差异表达基因。RT2 Profiler PCR Array用于研究toll样受体（TLR）通路相关基因的表达。我们发现CRNDE在星形胶质细胞中的过表达增加了toll样受体信号通路中关键因子的表达，特别是toll样受体3介导的MyD88非依赖性通路。此外，它上调下游转录因子如核因子κ B和许多细胞因子的表达水平。相反，在胶质瘤U87MG细胞系中CRNDE敲低显示上述基因表达的相反趋势。我们推测CRNDE可能通过toll样受体途径触发炎症反应来调节肿瘤的发生和发展。
Colorectal neoplasia differentially expressed (CRNDE), an oncogene, is highly expressed in many tumor cells and affects cellular proliferation, migration, invasion, and apoptosis. Its function and mechanism of action is a research hotspot. In this study, microarray analysis was performed to discover the differentially expressed genes in CRNDE over-expression cells. RT2 Profiler PCR Array was used to study the expression of genes related to the toll-like receptor (TLR) pathway. We found that over-expression of CRNDE in astrocytes increased the expression of key factors in the toll-like receptor signaling pathway, especially toll-like receptor-3-mediated MyD88-independent pathway. Furthermore, it up-regulated expression levels of downstream transcription factor such as nuclear factor kappa B and numerous cytokines. In contrast, CRNDE knockdown in glioma U87MG cell line showed an opposite trend in the expression of the above-mentioned genes. We speculated that CRNDE might trigger inflammation to regulate tumorigenesis and tumor development through the toll-like receptor pathway.