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Construction and analysis of a spinal cord injury competitive endogenous RNA network based on the expression data of long noncoding micro- and messenger RNAs

机译:基于长非编码微信使RNA表达数据的脊髓损伤竞争性内源RNA网络的构建和分析

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摘要

Spinal cord injury (SCI) results from trauma and predominantly affects the young male population. SCI imposes major and permanent life changes, and is associated with high future mortality and disability rates. Long non-coding RNAs (lncRNAs) have recently been demonstrated to serve critical roles in a broad range of biological processes and to be expressed in various diseases, including in SCI. However, the precise mechanisms underlying the roles of lncRNAs in SCI pathogenesis remain unexplored. In the present study, the aim was to identify critical differentially expressed lncRNAs in SCI based on the competing endogenous RNA (ceRNA) hypothesis by mining data from the Gene Expression Omnibus database of the National Center for Biotechnology Information and to unveil the functions of these lncRNAs. Different approaches and tools were employed to establish a network consisting of 13 lncRNA, 93 messenger RNA and 9 microRNA nodes, with a total of 202 edges. Three node lncRNAs were identified based on the degree distribution of the nodes, and their corresponding subnetworks were subsequently constructed. Based on these subnetworks, the biological pathways and interactions of these 3 lncRNAs were detailed using FunRich software (version 3.0). The primary results of the 3 lncRNA enrichment analyses were that they were associated with autophagy, extracellular communication and transcription factor networks, respectively. The phosphoinositide 3-kinase/protein kinase B/mammalian target of rapamycin signaling pathway of was the classic autophagy pathway, indicating that may regulate autophagy in SCI. The possible role of in SCI revealed in the current study based on the regulatory mechanism of ceRNAs has uncovered a new repertoire of molecular factors with potential as novel biomarkers and therapeutic targets in SCI.
机译:脊髓损伤(SCI)由外伤引起,主要影响年轻的男性人群。 SCI带来重大和永久性的生活变化,并与未来较高的死亡率和残障率相关。长的非编码RNA(lncRNA)最近已被证明在广泛的生物学过程中起关键作用,并在包括SCI在内的多种疾病中表达。但是,尚不清楚lncRNA在SCI发病机理中的作用的确切机制。在本研究中,目的是通过挖掘国家生物技术信息中心基因表达综合数据库的数据,并基于竞争性内源RNA(ceRNA)假设,确定SCI中关键的差异表达lncRNAs,并揭示这些lncRNA的功能。 。采用了不同的方法和工具来建立一个网络,该网络由13个lncRNA,93个Messenger RNA和9个microRNA节点组成,共有202条边。根据节点的程度分布确定了三个节点lncRNA,并随后构建了它们对应的子网。基于这些子网,使用FunRich软件(3.0版)详细介绍了这3个lncRNA的生物学途径和相互作用。 3种lncRNA富集分析的主要结果是它们分别与自噬,细胞外通讯和转录因子网络相关。雷帕霉素信号传导途径的磷酸肌醇3-激酶/蛋白激酶B /哺乳动物靶点是经典的自噬途径,表明可能调节SCI中的自噬。在当前研究中,基于ceRNAs调控机制的SCI在SCI中的可能作用揭示了一个新的分子因子库,这些分子因子可能是SCI中的新型生物标志物和治疗靶标。

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