The mechanisms and therapeutic potential of long noncoding RNA NEAT1 in fibrosis

Jiang, Xiaoying

doi:10.1007/s10238-023-01191-1

Clin Exp Med

2023

DOI: 10.1007/s10238-023-01191-1

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The mechanisms and therapeutic potential of long noncoding RNA NEAT1 in fibrosis

Xiaoying Jiang

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2024

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Cited by 3 publications

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Inhibition of long non-coding RNA NEAT1 suppressed the epithelial mesenchymal transition through the miR-204-5p/Six1 axis in asthma

Li,

Guan

et al. 2024

PLoS ONE

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Background Asthma, a prevalent chronic respiratory condition, is characterized by airway remodeling. Long non-coding RNA (lncRNA) NEAT1 has been demonstrated to participate in airway fibrosis. Furthermore, the miR-204-5p/Six1 axis significantly influences epithelial mesenchymal transition (EMT). However, the function of NEAT1/miR-204-5p/Six1 in asthmatic EMT remains unclear. Purpose This study intends to elucidate the function of NEAT1/miR-204-5p/Six1 axis in asthmatic EMT. Methods TGF-β1 was used to induce the EMT model in BEAS-2B cells. Immunofluorescence and western blot were executed to verify the establishment of the EMT model. NEAT1, miR-204-5p, and Six1 expression levels were evaluated using RT-qPCR. The role of NEAT1 in EMT in vitro was explored by CCK8 assays and flow cytometry. The luciferase reporter assay was performed to validate the interaction between NEAT1 and miR-204-5p/Six1. Results NEAT1 expression was increased during EMT. Functional experiments showed that the knockdown of NEAT1 suppressed cell proliferation and promoted cell apoptosis in vitro. Furthermore, inhibition of NEAT1 decreased the expression of N-cadherin, vimentin, and α-SMA and increased the expression of E-cadherin. Mechanistically, NEAT1 was identified as a sponge for miR-204-5p, and Six1 was found to be a direct target of miR-204-5p. Conclusion Down-regulation of NEAT1 reduced the Six1 expression via targeting miR-204-5p to inhibit the process of EMT in asthma. This study may provide new insight to reveal the underlying mechanisms of asthma.

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Inhibition of long non-coding RNA NEAT1 suppressed the epithelial mesenchymal transition through the miR-204-5p/Six1 axis in asthma

Li,

Guan

et al. 2024

PLoS ONE

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The potential therapeutic applications of long non-coding RNAs

Tamblin-Hopper,

Kiss-Toth,

Sudbery

et al. 2024

J Transl Genet Genom

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The field of RNA-based therapeutics is rapidly evolving and targeting non-coding RNAs (ncRNAs) associated with disease is becoming increasingly feasible. MicroRNAs (miRNAs) are a class of small ncRNAs (sncRNAs) and the first anti-miRNA drugs, e.g., Miravirsen and Cobomarsen, have successfully completed phase II clinical trials. Long ncRNAs (lncRNAs) are another class of ncRNAs that are commonly dysregulated in disease. Thus, they hold potential as putative therapeutic targets or agents. LncRNAs can function through a variety of mechanisms, including as guide, scaffold or decoy molecules, and understanding of these actions is critical to devising effective targeting strategies. LncRNA expression can be modulated with small interfering RNAs (siRNAs), antisense oligonucleotides (ASOs), CRISPR-Cas9, or small molecule inhibitors. These approaches have been employed to target a number of lncRNAs and tested in animal models of disease, including targeting ANRIL for non-small cell lung cancer and H19 for pancreatitis. However, there are currently no clinical trials registered in the ClinicalTrials.gov database that target lncRNAs as a therapeutic intervention. In order to translate lncRNA targeting into clinical use, several limitations must be overcome, such as potential toxicity and off-target effects. Overall, while significant progress has been made in the field, further development is required before the clinical application of the first therapeutics targeting lncRNAs. In this review, we discuss recent advances in our understanding of the mechanisms of action of lncRNAs that present avenues for clinical therapeutic targeting and consider off-target effects as a limiting factor in their application.

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Immunological characteristics of bronchoalveolar lavage fluid and blood across connective tissue disease-associated interstitial lung diseases

Hirano,

Sakashita,

Fujii

et al. 2024

Front. Immunol.

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Interstitial lung disease (ILD) is a serious complication of connective tissue diseases (CTDs). The heterogeneity of ILDs reflects differences in pathogenesis among diseases. This study aimed to clarify the characteristics of CTD-ILDs via a detailed analysis of the bronchoalveolar lavage fluid (BALF) and blood immune cells. BALF and blood samples were collected from 39 Japanese patients with newly diagnosed ILD: five patients with Sjögren’s syndrome (SS), eight patients with dermatomyositis (DM), six patients with rheumatoid arthritis (RA), six patients with systemic sclerosis, four patients with anti-neutrophil cytoplasmic antibody-associated vasculitis, and 10 patients with idiopathic interstitial pneumonia. We performed single-cell RNA sequencing to analyze the gene expression profiles in these patients’ immune cells. In patients with SS, B cells in the BALF were increased and genes associated with the innate and acquired immunity were enriched in both the BALF and blood. In contrast, patients with DM showed an upregulation of genes associated with viral infection in both the BALF and blood. In patients with RA, neutrophils in the BALF tended to increase, and their gene expression patterns changed towards inflammation. These disease-specific characteristics may help us understand the pathogenesis for each disease and discover potential biomarkers.

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The mechanisms and therapeutic potential of long noncoding RNA NEAT1 in fibrosis

Cited by 3 publications

References 45 publications

Inhibition of long non-coding RNA NEAT1 suppressed the epithelial mesenchymal transition through the miR-204-5p/Six1 axis in asthma

Inhibition of long non-coding RNA NEAT1 suppressed the epithelial mesenchymal transition through the miR-204-5p/Six1 axis in asthma

The potential therapeutic applications of long non-coding RNAs

Immunological characteristics of bronchoalveolar lavage fluid and blood across connective tissue disease-associated interstitial lung diseases

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