lncRNA PAN3-AS1 Modulates Cilium Assemble Signaling Pathway Through Regulation of RPGR as a Potential MS Diagnostic Biomarker: Integrated Systems Biology Investigation

IF 2.8 4区 医学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY
Yasaman Mostaghimi, Mohammad Haddadi, Zohreh Hojjati
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引用次数: 0

Abstract

Multiple sclerosis (MS), an autoimmune condition of the central nervous system (CNS), can lead to demyelination and axonal degeneration in the brain and spinal cord, which can cause progressive neurologic disability. MS symptoms include dysautonomia and progressive decline in motor abilities. In this investigation, we performed an integrated bioinformatics and experimental approach to find the expression level and interaction of a novel long non-coding RNA (lncRNA), PAN3-AS1, in MS samples. Microarray analysis was performed by R Studio using GEOquery and limma packages. lncRNA-mRNA RNA interaction analysis was performed using the lncRRIsearch database. Pathway enrichment analysis was performed by KEGG and Reactome online software through the Enrichr database. Protein–protein interaction analysis was performed by STRING online software. Gene ontology (GO) analysis was performed by Enrichr database. Based on microarray analysis, lncRNA PAN3-AS1 has a significantly low expression in MS samples compared to the control (logFC − 1.2, adj. P. Val 0.03). qRT-PCR results approved bioinformatics analyses. ROC analysis revealed that PAN3-AS1 could be considered a potential diagnostic biomarker of MS. Based on lncRNA-mRNA interaction analysis, lncRNA PAN3-AS1 regulates the expression level of RPGR. RPGR and its protein interactome regulate the cilium assembly, chaperon-mediated autophagy, and microarray biogenesis. lncRNA PAN3-AS1, as a significant low-expressed lncRNA in MS samples, could be a potential diagnostic MS biomarker. PAN3-AS1 might regulate the expression level of cilium assembly and chaperon-mediated autophagy. Dysregulation of PAN3-AS1 might affect the expression of RPGR and its protein interactome.

多发性硬化症(MS)是中枢神经系统(CNS)的一种自身免疫性疾病,可导致大脑和脊髓脱髓鞘和轴索变性,造成进行性神经残疾。多发性硬化症的症状包括自主神经功能障碍和运动能力进行性下降。在这项研究中,我们采用生物信息学和实验相结合的方法,寻找一种新型长非编码RNA(lncRNA)PAN3-AS1在多发性硬化症样本中的表达水平和相互作用。微阵列分析由R Studio使用GEOquery和limma软件包完成,lncRNA-mRNA RNA相互作用分析由lncRRIsearch数据库完成。通路富集分析由 KEGG 和 Reactome 在线软件通过 Enrichr 数据库进行。蛋白质-蛋白质相互作用分析由 STRING 在线软件进行。基因本体(GO)分析通过 Enrichr 数据库进行。根据微阵列分析,与对照组相比,lncRNA PAN3-AS1 在 MS 样本中的表达量明显较低(logFC - 1.2,adj. P. Val 0.03)。ROC分析显示,PAN3-AS1可被视为MS的潜在诊断生物标志物。基于lncRNA-mRNA相互作用分析,lncRNA PAN3-AS1调控RPGR的表达水平。RPGR及其蛋白相互作用组调控纤毛的组装、伴侣介导的自噬和微阵列的生物生成。lncRNA PAN3-AS1是多发性硬化症样本中一个重要的低表达lncRNA,可作为多发性硬化症的潜在诊断生物标志物。PAN3-AS1可能调控纤毛组装和伴侣介导的自噬的表达水平。PAN3-AS1的失调可能会影响RPGR及其蛋白相互作用组的表达。
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来源期刊
Journal of Molecular Neuroscience
Journal of Molecular Neuroscience 医学-神经科学
CiteScore
6.60
自引率
3.20%
发文量
142
审稿时长
1 months
期刊介绍: The Journal of Molecular Neuroscience is committed to the rapid publication of original findings that increase our understanding of the molecular structure, function, and development of the nervous system. The criteria for acceptance of manuscripts will be scientific excellence, originality, and relevance to the field of molecular neuroscience. Manuscripts with clinical relevance are especially encouraged since the journal seeks to provide a means for accelerating the progression of basic research findings toward clinical utilization. All experiments described in the Journal of Molecular Neuroscience that involve the use of animal or human subjects must have been approved by the appropriate institutional review committee and conform to accepted ethical standards.
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