Micro124-mediated AHR expression regulates the inflammatory response of chronic rhinosinusitis (CRS) with nasal polyps

Liu, C.C.; Xia, Mengna; Zhang, Y.J.; Jin, Ping; Zhao, Li; Zhang, J.; Li, T.; Zhou, Xiaoshuang; Tu, Yong-jiu; Kong, Feng; Sun, Caifeng; Shi, Lin; Zhao, Man

doi:10.1016/j.bbrc.2018.03.204

Cited by 35 publications

(36 citation statements)

References 23 publications

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“…This finding was consistent with previous reports that highlighted the link between miRs and inflammation in CRS [23]. Additionally, miR-124, for instance, has been demonstrated to target aryl hydrocarbon receptor to regulate inflammatory response in CRS [24]. Moreover, reports have suggested that LCN2 is highly expressed in episodes of inflammation and anti-bacterial responses [25] while silencing of LCN2 has been shown to alleviate inflammation in adipose tissues [26].…”

Section: Discussionsupporting

confidence: 92%

MicroRNA-761 suppresses remodeling of nasal mucosa and epithelial–mesenchymal transition in mice with chronic rhinosinusitis through LCN2

et al. 2020

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Background: Chronic rhinosinusitis (CRS) is characterized by persistent symptomatic inflammation of the nasal passage and sinus mucosa. Various microRNAs (miRs) have been implicated in CRS. Hence, the current study was conducted to explore the effect of microRNA-761 (miR-761) on remodeling of nasal mucosa and epithelial-mesenchymal transition (EMT).Methods: Bioinformatics analysis was initially performed to predict the differentially expressed genes (DEGs) associated with CRS. Gene targeting relationship between miR-761 and lipocalin 2 (LCN2) was analyzed by bioinformatics analysis and verified using dual-luciferase reporter gene assay. Histopathological analyses of the nasal mucosa tissues were conducted via hematoxylin-eosin (HE) and alcian blue (AB)-periodic acid Schiff (PAS) staining. ELISA was employed to determine the IL-8 and MMP-9 levels. To define downstream pathway of miR-761, levels of proteins related to LCN2/Twist1 signaling pathway were assessed. Additionally, the effects of miR-761 on EMT, proliferation, and apoptosis were determined.Results: LCN2 was highly expressed in CRS. LCN2 was a target of miR-761. miR-761 overexpression or LCN2 silencing decreased IL-8 and MMP-9 levels and morphological changes in nasal epithelial tissue from CRS mice. Overexpressed miR-761 or silenced LCN2 decreased the expression of LCN2 and Twist1, indicating LCN2/Twist1 signaling pathway was inactivated. Moreover, miR-761 overexpression or LCN2 silencing reduced the expression of N-cadherin and vimentin, while increased that of E-cadherin, suggesting inhibition of EMT. Furthermore, miR-761 overexpression or LCN2 silencing promoted cell proliferation and inhibited cell apoptosis in CRS.Conclusion: Taken together, miR-761 suppressed the remodeling of nasal mucosa through inhibition of LCN2 and the LCN2/Twist1 signaling pathway.

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Section: Discussionsupporting

confidence: 92%

MicroRNA-761 suppresses remodeling of nasal mucosa and epithelial–mesenchymal transition in mice with chronic rhinosinusitis through LCN2

et al. 2020

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“…As miRNAs have become a hot spot in the field of disease research, there is much evidence showing that miRNAs play a crucial role in a variety of biological processes . miR‐124 is abnormally expressed in inflammatory diseases (chronic sinusitis, ulcerative colitis) and immune disorders (rheumatoid arthritis) and acts as an inflammation response inhibitor . Moreover, it has been documented that miR‐124 has a wide range of biological effects and is involved in cell proliferation, autophagy, and neuronal differentiation .…”

Section: Biological Functions Of Mir‐124mentioning

confidence: 99%

“…9 miR-124 is abnormally expressed in inflammatory diseases (chronic sinusitis, ulcerative colitis) and immune disorders (rheumatoid arthritis) and acts as an inflammation response inhibitor. [10][11][12] Moreover, it has been documented that miR-124 has a wide range of biological effects and is involved in cell F I G U R E 1 The precoding flow chart of mature miR-124 proliferation, autophagy, and neuronal differentiation. [13][14][15] For instance, miR-124-3p has a significant neuroprotective function in Alzheimer's disease (AD) by targeting Caveolin-1 directly.…”

Section: Mir-124mentioning

confidence: 99%

MicroRNA‐124: An emerging therapeutic target in cancer

et al. 2019

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MicroRNAs (miRNAs) are noncoding single‐stranded RNAs, approximately 20‐24 nucleotides in length, known as powerful posttranscriptional regulators. miRNAs play important regulatory roles in cellular processes by changing messenger RNA expression and are widely involved in human diseases, including tumors. It has been reported in the literature that miRNAs have a precise role in cell proliferation, programmed cell death, differentiation, and expression of coding genes. MicroRNA‐124 (miR‐124) has reduced exparession in various human neoplasms and is believed to be related to the occurrence, development, and prognosis of malignant tumors. In our review, we focus on the specific molecular functions of miR‐124 and the downstream gene targets in major cancers, which provide preclinical evidence for the treatment of human cancer. Although some obstacles exist, miR‐124 is still attracting intensive research focus as a promising and effective anticancer weapon.

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“…At present, only a few articles have reported the relationship between ncRNA and CRSwNP, mainly focusing on miRNA [17,22], while lncRNA has not been addressed. ceRNA has important biological significance in many diseases, including cancer [23] and noncancer diseases [24].…”

Section: Discussionmentioning

confidence: 99%

Identification of Key Modules, Hub Genes, and Noncoding RNAs in Chronic Rhinosinusitis with Nasal Polyps by Weighted Gene Coexpression Network Analysis

Zhou

Zhen

Liu

et al. 2020

BioMed Research International

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Chronic rhinosinusitis with nasal polyps (CRSwNP) is a chronic inflammatory disease with relatively easy recurrence. However, the precise molecular mechanisms of this disease are poorly known. Based on gene sequencing data obtained from the Gene Expression Omnibus (GEO) database, we constructed coexpression networks by weighted gene coexpression network analysis (WGCNA). Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses were performed by the Database for Annotation, Visualization, and Integrated Discovery (DAVID). The core gene of pathogenesis, CRSwNP, was screened by protein-protein interaction data (PPI) from the HPRD database. Unsupervised clustering was applied to screen hub genes related to the phenotype of CRSwNP. Blue and turquoise modules were found to be most significantly related to the pathogenicity of CRSwNP. Functional enrichment analysis showed that cell proliferation in the blue modules, the apoptotic process in the turquoise module, and the cancer pathway in both modules were mostly significantly correlated with the development of CRSwNP. The noncoding RNAs (long noncoding RNA and microRNA) and the top 10 core genes in each module were found to be associated with the pathogenesis of CRSwNP. A total of nine hub genes were identified to be related to the CRSwNP phenotype. By qRT-PCR analysis, AKT1, CDH1, PIK3R1, CBL, LRP1, MALAT1, and XIST were proven to be associated with the pathogenesis of CRSwNP. AGR2, FAM3D, PIP, DSE, and TMC were identified to be related to the CRSwNP phenotype. Further exploration of these genes will reveal more important information about the mechanisms of CRSwNP.

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Micro124-mediated AHR expression regulates the inflammatory response of chronic rhinosinusitis (CRS) with nasal polyps

Cited by 35 publications

References 23 publications

MicroRNA-761 suppresses remodeling of nasal mucosa and epithelial–mesenchymal transition in mice with chronic rhinosinusitis through LCN2

MicroRNA-761 suppresses remodeling of nasal mucosa and epithelial–mesenchymal transition in mice with chronic rhinosinusitis through LCN2

MicroRNA‐124: An emerging therapeutic target in cancer

Identification of Key Modules, Hub Genes, and Noncoding RNAs in Chronic Rhinosinusitis with Nasal Polyps by Weighted Gene Coexpression Network Analysis

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