Knockdown CRNDE alleviates LPS-induced inflammation injury via FOXM1 in WI-38 cells

Zhuge, Dong; Yang, Yuping; Jiang, Zijun

doi:10.1016/j.biopha.2018.04.192

Cited by 33 publications

(26 citation statements)

References 41 publications

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“…More importantly, JAK/STAT and NF‐κB signalling has been implicated in pneumonia. For example, miR‐1247 could aggravate acute pneumonia through activating JNK and NF‐κB pathways, and CRNDE can upregulate FOXM1 that further activates NF‐κB and JAK/STAT pathways in LPS‐injured WI‐38 cells . Because of the key function of JAK/STAT and NF‐κB in pneumonia, our data prove that XIST knockdown contributes to inhibition of JAK/STAT and NF‐kB pathways through sponging miR‐370‐3p during pneumonia progression.…”

Section: Discussionmentioning

confidence: 58%

“…The release of inflammatory factors, such as TNF‐α, could promote cell apoptosis, microvascular dysfunction, and tissue necrosis . The cumulative message of several recent studies has revealed that lncRNAs are abnormally involved in inflammation response and serve as effective therapeutic targets for pneumonia . We put forward biological functions and mechanisms of XIST in pneumonia and firstly found that XIST knockdown lead to the inhibition of cell apoptosis and inflammation injuries in LPS‐induced WI‐38 cells by sponging miR‐370‐3p.…”

Section: Discussionmentioning

confidence: 99%

“…Cells (2 × 10 5 ) were plated in 6‐well plates and incubated 24 hours. LPS in different concentrations (5, 10, and 20 μg/mL) was added in medium for 12 hours to establish injury model …”

Section: Methodsmentioning

confidence: 99%

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Knockdown XIST alleviates LPS‐induced WI‐38 cell apoptosis and inflammation injury via targeting miR‐370‐3p/TLR4 in acute pneumonia

Zhang

Zhu

Gao

et al. 2019

Cell Biochemistry & Function

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Pneumonia is an inflammatory disease that occurs in the lungs associated with pathogens or other factors. It has been well established that long noncoding RNA X inactivate‐specific transcript (XIST) is involved in several cancers. The present study focused on the effect and detailed mechanism of XIST in lipopolysaccharide (LPS)‐induced injury in pneumonia. Here, XIST was silenced by transfection with XIST‐targeted siRNA, and then, mRNA expression, cell viability, apoptosis, and protein expression were, respectively, assessed by qRT‐PCR, CCK‐8, flow cytometry, and Western blotting. Luciferase reporter, RIP, and RNA pull‐down assays were used to detect the combination of miR‐370‐3p and XIST. Besides, the tested proinflammatory factors were analysed by qRT‐PCR and Western blot, and their productions were quantified by ELISA. The results showed that XIST expression was robustly increased in serum of patients with acute‐stage pneumonia and LPS‐induced WI‐38 human lung fibroblasts cells. Functional analyses demonstrated that knockdown of XIST remarkably alleviated LPS‐induced cell injury through increasing cell viability and inhibiting apoptosis and inflammatory cytokine levels. Mechanistically, XIST functioned as a competitive endogenous RNA (ceRNA) by effectively binding to miR‐370‐3p and then restoring TLR4 expression. More importantly, miR‐370‐3p inhibitor abolished the function of XIST knockdown on cell injury and JAK/STAT and NF‐κB pathways. Taken together, XIST may be involved in progression of cell inflammatory response, and XIST/miR‐370‐3p/TLR4 axis thus may shed light on the development of novel therapeutics to the treatment of acute stage of pneumonia. Significance of the study Our study demonstrated that XIST was highly expressed in patients with acute stage of pneumonia. Knockdown of XIST remarkably alleviated LPS‐induced cell injury through increasing cell viability and inhibiting apoptosis and inflammatory cytokine levels through regulating JAK/STAT and NF‐κB pathways.

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Section: Discussionmentioning

confidence: 58%

Section: Discussionmentioning

confidence: 99%

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Knockdown XIST alleviates LPS‐induced WI‐38 cell apoptosis and inflammation injury via targeting miR‐370‐3p/TLR4 in acute pneumonia

Zhang

Zhu

Gao

et al. 2019

Cell Biochemistry & Function

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“…Some studies highlight the significance of CRNDE in diverse diseases. For instance, CRNDE enhances hepatocellular carcinoma progression via upregulating SIX1; CRNDE accelerates LPS‐induced apoptosis and inflammation via upregulating FOXM1 in WI‐38 cells . In this study, the role of CRNDE in sepsis‐induced AHI was studied in vitro and in vivo.…”

Section: Discussionmentioning

confidence: 99%

“…It is worth noting that abnormally expressed CRNDE is linked to inflammatory response and apoptosis. For instance, upregulation of CRNDE overexpression accelerated lipopolysaccharide (LPS)‐induced apoptosis and inflammation via upregulation of forkhead box M1(FOXM1) in WI‐38 cells . In addition, CRNDE might trigger inflammation to regulate tumorigenesis and tumor development through the toll‐like receptor pathway .…”

Section: Introductionmentioning

confidence: 99%

Long noncoding RNA colorectal neoplasia differentially expressed alleviates sepsis‐induced liver injury via regulating miR‐126‐5p

Song²,

Xie

et al. 2020

IUBMB Life

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In this study, we intended to determine the detailed function and mechanism of long noncoding RNA (lncRNA) colorectal neoplasia differentially expressed (CRNDE) in liver injury induced by sepsis. Cecal ligation and perforation (CLP) models were adopted to induce sepsis in vivo with rats, and hepatic epithelial cells L02 were treated with lipopolysaccharide (LPS) to mimic sepsis in vitro. Enzyme‐linked immunosorbent assay was conducted to detect the levels of tumor necrosis factor (TNF‐α), interleukin‐6 (IL‐6), interleukin‐10 (IL‐10), and interferon‐γ (IFN‐γ) in the serum of rats. Quantitative real‐time polymerase chain reaction (qRT‐PCR) was performed to measure the expressions of CRNDE and microRNA‐126‐5p (miR‐126‐5p). Flow cytometry analysis and Cell Counting Kit‐8 (CCK‐8) method were carried out followed by the up‐ or downregulation of CRNDE and miR‐126‐5p to monitor the proliferation and apoptosis of L02 cells, respectively. Western blot was then applied to determine the expressions of cysteinyl aspartate specific proteinase 3 (caspase 3), poly(ADP‐ribose)polymerase (PARP), cytochrome c, and BCL2‐like 2 (BCL2L2). The interactions between CRNDE with miR‐126‐5p and miR‐126‐5p with BCL2L2 were determined through bioinformatics, qRT‐PCR, dual luciferase reporter assay, and RNA immunoprecipitation assay. CRNDE was significantly decreased in liver tissues and hepatic cells in sepsis models. Upregulation of CRNDE promoted the viability of L02 cells and inhibited their apoptosis, while downregulation of CRNDE had opposite effects. The expression of CRNDE in liver tissues of septic rats was correlated with the expression miR‐126‐5p. It was also demonstrated that the transfection of miR‐126‐5p mimics reversed the inhibitory effect induced by CRNDE on apoptosis of L02 cells. CRNDE could specifically bind to miR‐126‐5p and reduce its expression, in turn promote the expression of BCL2L2. Additionally, CRNDE overexpression in rats ameliorated liver injury induced by sepsis. Downregulated CRNDE aggravates hepatic injury via regulating miR‐126‐5p and BCL2L2 during sepsis.

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Thiostrepton: multifaceted biological activities and its applications in treatment of inflammatory diseases

Asikaer,

Sun,

Shen

2024

Inflammopharmacol

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Knockdown CRNDE alleviates LPS-induced inflammation injury via FOXM1 in WI-38 cells

Cited by 33 publications

References 41 publications

Knockdown XIST alleviates LPS‐induced WI‐38 cell apoptosis and inflammation injury via targeting miR‐370‐3p/TLR4 in acute pneumonia

Knockdown XIST alleviates LPS‐induced WI‐38 cell apoptosis and inflammation injury via targeting miR‐370‐3p/TLR4 in acute pneumonia

Long noncoding RNA colorectal neoplasia differentially expressed alleviates sepsis‐induced liver injury via regulating miR‐126‐5p

Thiostrepton: multifaceted biological activities and its applications in treatment of inflammatory diseases

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