Analysis of competing endogenous RNA (ceRNA) crosstalk in eosinophilic chronic rhinosinusitis with nasal polyps

被引:3
|
作者
Li, Ke [1 ]
Liu, Fang-Fang [2 ]
机构
[1] Huazhong Univ Sci & Technol, Tongji Hosp, Tongji Med Coll, Dept Blood Transfus, Wuhan, Peoples R China
[2] Huazhong Univ Sci & Technol, Cent Hosp Wuhan, Tongji Med Coll, Dept Pathol, Wuhan 430014, Peoples R China
基金
中国国家自然科学基金;
关键词
ceRNA crosstalk; CRSwNP; eosinophilic CRSwNP; GSEA; ncRNA; NONCODING RNAS; DATABASE; EXPRESSION; NETWORKS;
D O I
10.1002/alr.23008
中图分类号
R76 [耳鼻咽喉科学];
学科分类号
100213 ;
摘要
Background Chronic rhinosinusitis with nasal polyps (CRSwNP) is one of the most common chronic inflammatory diseases, and has various phenotypes. Although its pathophysiology remains obscure, evidence has shown that dysregulation of noncoding RNAs (ncRNAs) is associated with CRSwNP. ncRNAs in the cytoplasm can act as competing endogenous RNAs (ceRNAs), which are involved in many inflammatory processes. However, the ceRNA crosstalk in CRSwNP is still unclear Methods We investigated expression profiles of messenger RNA (mRNA), microRNAs (miRNAs), and long noncoding RNAs (lncRNAs) in eosinophilic CRSwNP and constructed a global triple ceRNA network. Results As a result, 964 differentially expressed mRNAs (DEmRs), 207 differentially expressed miRNAs (DEmiRs), and 15 differentially expressed lncRNAs (DElncRs) were identified, and a ceRNA network containing 598 miRNA-mRNA pairs and 70 lncRNA-miRNA pairs was finally constructed. Gene set enrichment analysis (GSEA) results indicated these DEmRs were mainly enriched in "cytokine-cytokine receptor interaction," "salivary secretion," "hematopoietic cell lineage," and "chemokine signaling pathway." Moreover, we also predicted the subcellular localization of the DElncRs identified in the network via bioinformatics approaches Conclusion In summary, the present study provided the first comprehensive assessment of the ceRNA crosstalk in eosinophilic CRSwNP. These findings will be of interest to the understanding of the potential pathophysiology of this disease.
引用
收藏
页码:1468 / 1479
页数:12
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