<i>Retracted:</i> Protective impacts of circular RNA VMA21 on lipopolysaccharide‐engendered WI‐38 cells injury via mediating microRNA‐142‐3p

Yang, Pei-li; Gao, Ran; Zhou, Wenwen; Han, Anbang

doi:10.1002/biof.1593

Cited by 25 publications

(14 citation statements)

References 29 publications

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“…For instance, Yang et al . reported that circRNA vacuolar ATPase assembly factor (circVMA21) protected WI‐38 cell from lipopolysaccharide (LPS)‐triggered inflammatory injury possibly by regulating microRNA (miRNA)‐142‐3p and nuclear factor‐κB (NF‐κB) signaling . Guo and colleagues revealed that the knockdown of circRNA ankyrin repeat domain 36 (circANKRD36) relieved LPS‐evoked cytotoxicity in MRC‐5 cells via sponging miRNA‐31 and regulating myeloid differentiation factor 88 (MyD88) .…”

Section: Introductionmentioning

confidence: 99%

Circ_0038467 regulates lipopolysaccharide‐induced inflammatory injury in human bronchial epithelial cells through sponging miR‐338‐3p

Liu

Wan

et al. 2020

Thoracic Cancer

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Background: Pneumonia is a common acute lower respiratory infection in children and elders. Circular RNAs (circRNAs) have recently been uncovered to play important roles in pneumonia. However, the function and mechanism of circ_0038467 in pneumonia remain elusive. Methods: Cell viability and apoptosis were determined using the Cell Counting Kit-8 (CCK-8) assay and flow cytometry, respectively. The levels of interleukin 6 (IL-6), IL-8 and IL-1β were detected by enzyme-linked immunosorbent assay (ELISA). Western blot analysis was performed to assess the expression of related proteins. Circ_0038467 was characterized by Ribonuclease R (RNase) digestion and subcellular localization assays. The levels of circ_0038467 and miR-338-3p were evaluated by quantitative real-time polymerase chain reaction (qRT-PCR). The direct interaction between circ_0038467 and miR-338-3p was validated by the dual-luciferase reporter and RNA immunoprecipitation (RIP) assays. Results: Our data indicated that lipopolysaccharide (LPS) induced an inflammatory injury in 16HBE cells by repressing cell viability and enhancing cell apoptosis and proinflammatory cytokines production. Circ_0038467 was upregulated and miR-338-3p was downregulated in LPS-treated 16HBE cells. Circ_0038467 knockdown or miR-338-3p overexpression attenuated LPS-induced 16HBE cell inflammatory injury. Moreover, circ_0038467 acted as a sponge of miR-338-3p in 16HBE cells. MiR-338-3p mediated the alleviated effect of circ_0038467 knockdown on LPS-induced 16HBE cell inflammatory injury. Additionally, the Janus kinase/ signal transducer and activator of transcription 3 (JAK/STAT3) signaling pathway was involved in the circ_0038467/miR-338-3p axis-mediated regulation in LPS-induced 16HBE cell inflammatory injury. Conclusions: The current work had led to the identification of circ_0038467 knockdown that alleviated LPS-induced inflammatory injury in 16HBE cells at least partly through sponging miR-338-3p and regulating JAK/STAT3 pathway, highlighting novel molecular targets for the treatment of pneumonia.

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Section: Introductionmentioning

confidence: 99%

Circ_0038467 regulates lipopolysaccharide‐induced inflammatory injury in human bronchial epithelial cells through sponging miR‐338‐3p

Liu

Wan

et al. 2020

Thoracic Cancer

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“…In addition, NCI-H1650 cells were transfected with miR-767-3p agonist, miR-767-3p antagonist or negative control (NC) RNAs (GenePharma, Shanghai, China) using Lipofectamine 2000 as previously described [35]. The transfection efficiency was determined using q-PCR.…”

Section: Cell Transfectionmentioning

confidence: 99%

Hsa_circ_0018818 knockdown suppresses tumorigenesis in non-small cell lung cancer by sponging miR-767-3p

Zhou

Gao

et al. 2020

Aging

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To identify potential therapeutic targets in non-small cell lung cancer NSCLC, we conducted a bioinformatics analysis of circRNAs differentially expressed between NSCLC tissues and adjacent normal tissues. Cell proliferation and apoptosis was assessed using CCK-8 and flow cytometry, respectively. A connection between hsa_circ_0018818 and miR-767-3p was confirmed in dual luciferase reporter assays. Gene and protein expression in NSCLC cells were measured using quantitative PCR and Western-blotting, respectively. And a xenograft tumor model was established to assess the function of hsa_circ_0018818 in NSCLC in vivo. Hsa_circ_0018818 was greatly upregulated in NSCLC tumor tissues. Knocking down hsa_circ_0018818 using a targeted shRNA inhibited the proliferation and invasiveness of NSCLC cells and induced their apoptosis via the miR-767-3p/Nidogen 1 (NID1) signaling axis. Hsa_circ_0018818 knockdown also inactivated Epithelialmesenchymal transition (EMT) process and PI3K/Akt signaling. In summary, hsa_circ_0018818 knockdown inhibited NSCLC tumorigenesis in vitro and in vivo, which suggests it could potentially serve as a target for the treatment of NSCLC.

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“…Cheng et al (2018) reported that circRNA vacuolar ATPase assembly factor (circ_VMA21, hsa_circ_0091702) inhibited the inflammatory cytokines-induced intervertebral disc degeneration by regulating the miR-200c/XIAP pathway. Yang et al (2020) found circ_VMA21 protected against the LPS-induced pneumonia by targeting miR-142-3p.…”

Section: Introductionmentioning

confidence: 96%

circ_VMA21 protects WI-38 cells against LPS-induced apoptotic and inflammatory injury by acting on the miR-409-3p/KLF4 axis

Wang¹,

Zhang²,

Chen³

2021

gpb

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Highlights1. circ_VMA21 ameliorates LPS-induced WI-38 cellular apoptosis and inflammation 2. circ_VMA21 targets miR-409-3p and KLF4 is a target of miR-409-3p 3. circ_VMA21 promotes the expression of KLF4 via sponging miR-409-3p Abstract. Pneumonia is a common inflammatory lung disease. Circular RNA (circRNA) vacuolar ATPase assembly factor (circ_VMA21) has been reported to mitigate the inflammatory injury in WI-38 cells. This study was to investigate the functional mechanism of circ_VMA21. Cell model was established by lipopolysaccharide (LPS) treatment in WI-38 cells. Cell cycle and apoptosis were analyzed by flow cytometry. Cell proliferation was assessed by colony formation and MTT assays. The expression quantification of circ_VMA21, microRNA-409-3p (miR-409-3p) and Kruppel-like transcription factor 4 (KLF4) was performed by qRT-PCR method. The expression of relative protein was detected by Western blot. Inflammatory response was evaluated by ELISA. The target binding was validated by dual-luciferase reporter assay. Cellular analysis indicated that LPS repressed cell cycle and proliferation but induced apoptosis. circ_VMA21 was downregulated in pneumonia samples and LPS-treated WI-38 cells. Functionally, circ_VMA21 assuaged the LPS-induced apoptotic and inflammatory damages. In addition, circ_VMA21 directly targeted miR-409-3p and its function was dependent on the sponge effect on miR-409-3p. Also, KLF4 was a target of miR-409-3p and miR-409-3p inhibitor attenuated LPS-induced cell injury by upregulating KLF4. Moreover, KLF4 was upregulated by circ_VMA21/miR-409-3p axis. These findings suggested that circ_VMA21 relieved the LPS-induced apoptotic and inflammatory injury by the regulation of miR-409-3p/KLF4 axis.

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Retracted: Protective impacts of circular RNA VMA21 on lipopolysaccharide‐engendered WI‐38 cells injury via mediating microRNA‐142‐3p

Cited by 25 publications

References 29 publications

Circ_0038467 regulates lipopolysaccharide‐induced inflammatory injury in human bronchial epithelial cells through sponging miR‐338‐3p

Circ_0038467 regulates lipopolysaccharide‐induced inflammatory injury in human bronchial epithelial cells through sponging miR‐338‐3p

Hsa_circ_0018818 knockdown suppresses tumorigenesis in non-small cell lung cancer by sponging miR-767-3p

circ_VMA21 protects WI-38 cells against LPS-induced apoptotic and inflammatory injury by acting on the miR-409-3p/KLF4 axis

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