LncRNA SNHG16 promotes pulmonary fibrosis by targeting miR-455-3p to regulate the Notch2 pathway

Li, Panpan; Zhao, Lei; Gu, Yuxia; Zhang, Meilan; Gao, Hongchang; Meng, Yingxia

doi:10.1186/s12931-021-01632-z

Cited by 15 publications

(14 citation statements)

References 37 publications

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“…For example, lncRNA Hoxaas3 accelerates pulmonary fibrosis by targeting the miR-450b-5p/Runx1 axis ( 22 ). Liu et al found that lncRNA SNHG16 also functions as a promoter in pulmonary fibrosis via the modulation of the Notch2 pathway ( 12 ). Sun et al showed that lncRNA pulmonary fibrosis inhibitor (PFI) ameliorates pulmonary fibrosis by binding to splicing regulator Serine/arginine-rich splicing factor 1 (SRSF1) ( 14 ).…”

Section: Discussionmentioning

confidence: 99%

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The silencing of lnc-NONHSAT071210 suppresses the proliferation, fibrosis, migration, and invasion of TGFβ1-treated lung epithelial cells

Liu¹,

Fj²,

Li³

et al. 2022

Ann Transl Med

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Background: Pulmonary fibrosis, which is a frequent manifestation of connective tissue disease (CTD), is a leading cause of morbidity and mortality. However, the role of long non-coding ribonucleic acids (lncRNAs) in CTD-associated pulmonary fibrosis requires clarification. This study sought to examine the effects of lnc-NONHSAT071210 on the phenotypes of transforming growth factor β1 (TGFβ1)-treated lung epithelial cells. Methods:The GeneChip was used to identify differentially expressed lncRNAs in CTD-associated pulmonary fibrosis patients. After lnc-NONHSAT071210 was knocked down in the TGFβ1-challenged lung epithelial cells, cell viability, cell cycle, migration, and invasion were estimated by Cell Counting Kit-8 assays, a flow cytometry analysis, wound-healing assays, and transwell assays, respectively. The expression and levels of the fibrosis-associated factors were examined by enzyme-linked immunosorbent assays, RT-qPCR, and western blots. Results:The expression of the top 7 most significantly upregulated lncRNAs in the CTD-associated pulmonary fibrosis patients was depicted in a heat map and examined by reverse transcription-quantitative polymerase chain reaction (RT-qPCR). The results showed that the expression of lnc-NONHSAT071210 was significantly increased in the tissues of the CTD-associated pulmonary fibrosis patients (P<0.001). The silencing of Lnc-NONHSAT071210 suppressed proliferation, migration, and invasion in the TGFβ1exposed alveolar epithelial cells (P<0.001).Conclusions: Thus, lnc-NONHSAT071210 expression was increased in the tissues of the CTD-associated pulmonary fibrosis patients and TGFβ1-treated lung epithelial cells, and TGFβ1-induced lung epithelial cell injury was alleviated by impeding the expression of lnc-NONHSAT071210.

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Section: Discussionmentioning

confidence: 99%

“…Several lncRNAs have been shown to have important functions in the pathogenesis of systemic sclerosis, dermatomyositis, and cutaneous lupus erythematosus (11). Notably, lncRNAs have been shown to participate in pulmonary fibrosis (12)(13)(14). Lnc-NONHSAT071210 is a novel lncRNA on which little research has been conducted to date.…”

Section: Introductionmentioning

confidence: 99%

The silencing of lnc-NONHSAT071210 suppresses the proliferation, fibrosis, migration, and invasion of TGFβ1-treated lung epithelial cells

Liu¹,

Fj²,

Li³

et al. 2022

Ann Transl Med

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“…SNHG16 is an important tumour-associated lncRNA that regulates many miRNAs, including miR-216-5p [148], miR-455-3p [149], and miR-605-3p [150]. A 7571bp region encodes it on chromosome 17q25.1.…”

Section: Snhg16mentioning

confidence: 99%

Long noncoding RNAs: glycolysis regulators in gynaecologic cancers

Shen

Chen

et al. 2023

Cancer Cell Int

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The three most common gynaecologic cancers that seriously threaten female lives and health are ovarian cancer, cervical cancer, and endometrial cancer. Glycolysis plays a vital role in gynaecologic cancers. Several long noncoding RNAs (lncRNAs) are known to function as oncogenic molecules. LncRNAs impact downstream target genes by acting as ceRNAs, guides, scaffolds, decoys, or signalling molecules. However, the role of glycolysis-related lncRNAs in regulating gynaecologic cancers remains poorly understood. In this review, we emphasize the functional roles of many lncRNAs that have been found to promote glycolysis in gynaecologic cancers and discuss reasonable strategies for future research.

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“…Increasing evidence shows that long noncoding RNAs (lncRNAs) have an important influence on PF [ 12 , 13 ]. Gokey et al [ 14 ] showed that in IPF epithelial cells, the most improved lncRNA is lncRNA maternally expressed gene 3 (MEG3), which plays an important role in regulating the function of basic progenitor cells.…”

Section: Introductionmentioning

confidence: 99%

IL-27 induces autophagy through regulation of the DNMT1/lncRNA MEG3/ERK/p38 axis to reduce pulmonary fibrosis

Yang

Zhou

et al. 2023

Respir Res

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Purpose Previous studies have shown that interleukin-27 (IL-27) can reduce bleomycin (BLM)-induced pulmonary fibrosis (PF). However, the underlying mechanism by which IL-27 attenuates PF is not fully clear. Methods In this research, we used BLM to construct a PF mouse model, and MRC-5 cells stimulated by transforming growth factor-β1 (TGF-β1) were used to construct a PF model in vitro. The lung tissue status was observed by Masson and hematoxylin and eosin (HE) staining. To detect gene expression, RT‒qPCR was used. The protein levels were detected by western blotting and immunofluorescence staining. EdU and ELISA were used to detect cell proliferation viability and hydroxyproline (HYP) content, respectively. Results Aberrant IL-27 expression was observed in BLM-induced mouse lung tissues, and the use of IL-27 attenuated mouse lung tissue fibrosis. TGF-β1 induced autophagy inhibition in MRC-5 cells, and IL-27 alleviated MRC-5 cell fibrosis by activating autophagy. The mechanism is inhibition of DNA methyltransferase 1 (DNMT1)-mediated lncRNA MEG3 methylation and ERK/p38 signaling pathway activation. Overexpression of DNMT1, knockdown of lncRNA MEG3, autophagy inhibitor or ERK/p38 signaling pathway inhibitors reversed the positive effect of IL-27 in a lung fibrosis model in vitro. Conclusion In conclusion, our study shows that IL-27 upregulates MEG3 expression through inhibition of DNMT1-mediated lncRNA MEG3 promoter methylation, which in turn inhibits ERK/p38 signaling pathway-induced autophagy and attenuates BLM-induced PF, providing a contribution to the elucidation of the potential mechanisms by which IL-27 attenuates PF.

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LncRNA SNHG16 promotes pulmonary fibrosis by targeting miR-455-3p to regulate the Notch2 pathway

Cited by 15 publications

References 37 publications

The silencing of lnc-NONHSAT071210 suppresses the proliferation, fibrosis, migration, and invasion of TGFβ1-treated lung epithelial cells

The silencing of lnc-NONHSAT071210 suppresses the proliferation, fibrosis, migration, and invasion of TGFβ1-treated lung epithelial cells

Long noncoding RNAs: glycolysis regulators in gynaecologic cancers

IL-27 induces autophagy through regulation of the DNMT1/lncRNA MEG3/ERK/p38 axis to reduce pulmonary fibrosis

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