<i>Retracted:</i> Circular RNA ANKRD36 attends to lipopolysaccharide‐aroused MRC‐5 cell injury via regulating microRNA‐31‐3p

Guo, Rui; Zhang, Lijuan; Meng, Jingjing

doi:10.1002/biof.1592

Cited by 33 publications

(22 citation statements)

References 38 publications

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“…MiR-31-3p was found to target MyD88, therefore downregulating the NF-κB pathway. Thus, apoptosis and ROS production observed in LPS-treated MRC5 were caused, at least in part, by the circANKRD36 binding with miR-31-3p that impeded the miRNA downregulation of the NF-κB pathway [199].…”

Section: Mirnas and Oxidative Stress In Both Cardiac And Pulmonary DImentioning

confidence: 97%

MicroRNA and ROS Crosstalk in Cardiac and Pulmonary Diseases

Climent

Viggiani

Lin

et al. 2020

IJMS

101

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Reactive oxygen species (ROS) affect many cellular functions and the proper redox balance between ROS and antioxidants contributes substantially to the physiological welfare of the cell. During pathological conditions, an altered redox equilibrium leads to increased production of ROS that in turn may cause oxidative damage. MicroRNAs (miRNAs) regulate gene expression at the post-transcriptional level contributing to all major cellular processes, including oxidative stress and cell death. Several miRNAs are expressed in response to ROS to mediate oxidative stress. Conversely, oxidative stress may lead to the upregulation of miRNAs that control mechanisms to buffer the damage induced by ROS. This review focuses on the complex crosstalk between miRNAs and ROS in diseases of the cardiac (i.e., cardiac hypertrophy, heart failure, myocardial infarction, ischemia/reperfusion injury, diabetic cardiomyopathy) and pulmonary (i.e., idiopathic pulmonary fibrosis, acute lung injury/acute respiratory distress syndrome, asthma, chronic obstructive pulmonary disease, lung cancer) compartments. Of note, miR-34a, miR-144, miR-421, miR-129, miR-181c, miR-16, miR-31, miR-155, miR-21, and miR-1/206 were found to play a role during oxidative stress in both heart and lung pathologies. This review comprehensively summarizes current knowledge in the field.

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Section: Mirnas and Oxidative Stress In Both Cardiac And Pulmonary DImentioning

confidence: 97%

MicroRNA and ROS Crosstalk in Cardiac and Pulmonary Diseases

Climent

Viggiani

Lin

et al. 2020

IJMS

101

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“…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) . As for circ_0038467, derived from the back‐splicing of ubiquinol‐cytochrome‐c reductase core protein 2 (UQCRC2), it was found to be significantly upregulated in neodymium oxide‐induced 16HBE cell line using the microarray circRNA analysis .…”

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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“…Therefore, circANKRD36 may be used as a biomarker for screening chronic inflammation in patients with T2DM (54) . Another study showed an association between pneumonia pathogenesis and circANKRD36 (55) . Irritated MRC-5 cell injury by lipopolysaccharide (LPS) evoked circANKRD36 to activate the NF-κB signaling pathway and caused inflammation in MRC-5 cells.…”

Section: Discussionmentioning

confidence: 99%

Integrated Genomic Analysis Identifies ANKRD36 Gene as a Novel and Common Biomarker of Disease Progression in Chronic Myeloid Leukemia

Iqbal¹,

Absar²,

Akhtar³

et al. 2021

Preprint

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Background: Chronic Myeloid Leukemia (CML) is initiated in bone marrow due to chromosomal translocation t(22;9) leading to fusion oncogene BCR-ABL. Targeting BCR-ABL by tyrosine kinase inhibitors (TKI) have changed fatal CML into an almost curable disease. Despite that, TKIs lose their effectiveness due to disease progression. Unfortunately, mechanism of CML progression is poorly understood and common biomarkers for CML progression are unavailable. This study was conducted to find out novel biomarkers of CML progression by employing whole exome sequencing (WES).Materials and Methods: WES of accelerated phase (AP-) and blast crisis (BC-) CML patients was carried out, with chronic phase CML (CP-CML) patients as control. After DNA library preparation and exome enrichment, clustering and sequencing was carried out using Illumina platforms. Statistical analysis was carried out using [SAS/STAT] software version 9.4 and R package employed to find mutations shared exclusively by all AP-/BC-CML. Confirmation of mutations was carried out using Sanger sequencing and protein structure modelling using I-Tasser followed by mutant generation and visualization using PyMOL. Results: Three novel genes (ANKRD36, ANKRD36B and PRSS3) were mutated exclusively in all AP-/BC-CML patients. Only ANKRD36 gene mutations (c.1183_1184 delGC and c.1187_1185 dupTT) were confirmed by Sanger sequencing. Protein modelling studies showed that mutations induce structural changes in ANKRD36 protein. Conclusions: Our studies show that ANKRD36 is a potential common biomarker and drug target of early CML progression. ANKRD36 is yet uncharacterized in human. It has the highest expression in bone marrow, specifically myeloid cells. We recommend carrying out further studies to explore the role of ANKRD36 in biology and progression of CML.

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Retracted: Circular RNA ANKRD36 attends to lipopolysaccharide‐aroused MRC‐5 cell injury via regulating microRNA‐31‐3p

Cited by 33 publications

References 38 publications

MicroRNA and ROS Crosstalk in Cardiac and Pulmonary Diseases

MicroRNA and ROS Crosstalk in Cardiac and Pulmonary Diseases

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

Integrated Genomic Analysis Identifies ANKRD36 Gene as a Novel and Common Biomarker of Disease Progression in Chronic Myeloid Leukemia

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