Long Noncoding RNA/Circular RNA-miRNA-mRNA Axes in Ischemia-Reperfusion Injury

Gong, Chengwu; Zhou, Xueliang; Lai, Songqing; Wang, Lijun; Liu, Jichun

doi:10.1155/2020/8838524

Cited by 27 publications

(18 citation statements)

References 150 publications

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“…Previous studies indicated that circRNA acts as an miRNA sponge through competitive binding, consequently leading to loss of function of target miRNA and affect gene expression at the post-transcriptional level (15)(16)(17)(18)(19). In the present study, the results of the luciferase reporter assay revealed the interaction between circ_0008932 and miR-145-5p.…”

Section: Discussionsupporting

confidence: 54%

Suppression of circ_0008932 inhibits tumor growth and metastasis in osteosarcoma by targeting miR‑145‑5p

Cao

Shu

2021

Exp Ther Med

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Osteosarcoma (OS) is a common type of primary malignant tumor. Although the pathogenesis of OS has been extensively studied, the underlying molecular mechanisms have remained to be fully elucidated. Accumulating evidence has revealed that dysregulation of various circular RNAs (circRNAs) is associated with tumorigenesis and recent studies have indicated that circRNA circ_0008932 is aberrantly expressed in tumors. In the present study, the expression and detailed function of circ_0008932 in OS were elucidated. The levels of circ_0008932 in OS samples and cell lines were examined using reverse transcription-quantitative PCR. A cell model with circ_0008932 knockdown was generated using specific small interfering RNA (si-circ_0008932). Cell viability was determined by a Cell Counting Kit-8 assay, the cell migratory/invasive capacity was evaluated using Transwell assays and cell apoptosis was assessed by flow cytometry. The results suggested that circ_0008932 was upregulated in most primary OS tumors, suggesting that circ_0008932 is associated with the development of OS. In the in vitro assays, si-circ_0008932 inhibited the proliferation, migration and invasion of OS cells, while apoptosis was promoted. A luciferase reporter assay revealed that circ_0008932 may downregulate microRNA (miR)-145-5p through direct binding. Furthermore, the expression of miR-145-5p was negatively correlated with circ_0008932 levels in OS specimens. In addition, further functional studies indicated that miR-145-5p inhibitors eliminated the effects caused by si-circ_0008932 in OS cells. In comparison, the changes in the biological behavior of OS cells transfected with si-circ_0008932 were enhanced by miR-145-5p. In summary, circ_0008932 may be a novel oncogenic factor during the progression and development of OS by targeting miR-145-5p; more importantly, circ_0008932 may be a potential therapeutic target for OS.

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Section: Discussionsupporting

confidence: 54%

Suppression of circ_0008932 inhibits tumor growth and metastasis in osteosarcoma by targeting miR‑145‑5p

Cao

Shu

2021

Exp Ther Med

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“…According to the admitted hypothesis, lncRNA indirectly regulates the mRNA expression by competitively interacting with miRNA ( Bao et al, 2018 ; Gong et al, 2020 ). In this article, we constructed our ceRNA network as follows ( Campbell and Khatri, 2020 ): predicting possible lncRNAs that interact with miRNA by using prediction modules of DIANA-LncBase Predicted V.2 database ( Paraskevopoulou et al, 2016 ) and forming pairwise relations between lncRNA and miRNA; the interacting score of prediction modules higher than 0.7 considered as eligible ( Donnan et al, 2008 ); miRWalk ( Dweep et al, 2011 ) 3.0, miRDB ( Chen and Wang, 2019 ), and TargetScan ( Agarwal et al, 2015 ) (Version 7.2), were used to predict the interaction between miRNAs and mRNAs, and the interacting score higher than 0.95 was regarded as eligible ( Emberson et al, 2014 ); lncRNAs and mRNAs predicted by previous two steps were matched with DElncRNAs and DEmRNAs, and only overlapped lncRNA–miRNA and mRNA–miRNA relationships were selected ( Kopp and Mendell, 2018 ); arranging these paired matched relationships, the ultimate lncRNA–miRNA–mRNA network was formed and visualized through Cytoscape (Version 3.8.0).…”

Section: Methodsmentioning

confidence: 99%

“…Long noncoding RNAs (lncRNAs) are defined as transcripts that are longer than 200 nucleotides and are unable to encode proteins ( Kopp and Mendell, 2018 ). They were previously considered as “junk” in the mammal genome but now are found to function as a transcriptional regulator or post-transcriptional regulator: in the former, lncRNA combines with chromosomes and modifies the gene expression ( Ulitsky and Bartel, 2013 ), whereas in the latter, lncRNA can either directly impact the gene expression by regulating the degradation of genes or works as competing endogenous RNA (ceRNA) and sponge-specific miRNAs, thus indirectly regulating the gene expression ( Bao et al, 2018 ; Gong et al, 2020 ). Recently, aberrant expression of lncRNA has been reported to correlate with the onset, progression, and prognosis of acute ischemic stroke (AIS) ( Bai et al, 2014 ; Feng et al, 2019 ; Li et al, 2020a ; Wang et al, 2020a ; Fu et al, 2021 ); thus they are potential candidates for stroke diagnosis.…”

Section: Introductionmentioning

confidence: 99%

Comprehensive Analysis of Hub Genes Associated With Competing Endogenous RNA Networks in Stroke Using Bioinformatics Analysis

Chen

2022

Front. Genet.

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Background: Acute ischemic stroke (AIS) is the second leading cause of death and the third leading cause of disability worldwide. Long noncoding RNAs (lncRNAs) are promising biomarkers for the early diagnosis of AIS and closely participate in the mechanism of stroke onset. However, studies focusing on lncRNAs functioning as microRNA (miRNA) sponges to regulate the mRNA expression are rare and superficial.Methods: In this study, we systematically analyzed the expression profiles of lncRNA, mRNA (GSE58294), and miRNA (GSE110993) from the GEO database. Gene ontology (GO) analysis was performed to reveal the functions of differentially expressed genes (DEGs), and we used weighted gene co-expression network analysis (WGCNA) to investigate the relationships between clinical features and expression profiles and the co-expression of miRNA and lncRNA. Finally, we constructed a lncRNA–miRNA–mRNA competing endogenous RNA (ceRNA) network with selected DEGs using bioinformatics methods and obtained ROC curves to assess the diagnostic efficacy of differentially expressed lncRNAs (DElncRNAs) and differentially expressed mRNAs (DEmRNAs) in our network. The GSE22255 dataset was used to confirm the diagnostic value of candidate genes.Results: In total, 199 DElncRNAs, 2068 DEmRNAs, and 96 differentially expressed miRNAs were detected. The GO analysis revealed that DEmRNAs primarily participate in neutrophil activation, neutrophil degranulation, vacuolar transport, and lysosomal transport. WGCNA screened out 16 lncRNAs and 195 mRNAs from DEGs, and only eight DElncRNAs maintained an area under the curve higher than 0.9. By investigating the relationships between lncRNAs and mRNAs, a ceRNA network containing three lncRNAs, three miRNAs, and seven mRNAs was constructed. GSE22255 confirmed that RP1-193H18.2 is more advantageous for diagnosing stroke, whereas no mRNA showed realistic diagnostic efficacy.Conclusion: The ceRNA network may broaden our understanding of AIS pathology, and the candidate lncRNA from the ceRNA network is assumed to be a promising therapeutic target and diagnostic biomarker for AIS.

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“…Furthermore, in different pathologies correlated with oxidative stress, these regulatory mechanisms have begun to take center stage [ 224 ] In I-R, miRNAs have great advantages when used as a therapeutic target. In the future, they could be considered pharmacological approaches in clinical practice [ 255 ]. Noncoding RNA similar to miR-92a has a proangiogenic effect, and miR-499 can decrease damage induced by hypoxia-reoxygenation.…”

Section: Ischemia-reperfusion Antioxidant Pharmacodynamicsmentioning

confidence: 99%

Therapeutic Targets for Regulating Oxidative Damage Induced by Ischemia-Reperfusion Injury: A Study from a Pharmacological Perspective

Rangel

García-Valdés

Villar

et al. 2022

Oxidative Medicine and Cellular Longevity

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Ischemia-reperfusion (I-R) injury is damage caused by restoring blood flow into ischemic tissues or organs. This complex and characteristic lesion accelerates cell death induced by signaling pathways such as apoptosis, necrosis, and even ferroptosis. In addition to the direct association between I-R and the release of reactive oxygen species and reactive nitrogen species, it is involved in developing mitochondrial oxidative damage. Thus, its mechanism plays a critical role via reactive species scavenging, calcium overload modulation, electron transport chain blocking, mitochondrial permeability transition pore activation, or noncoding RNA transcription. Other receptors and molecules reduce tissue and organ damage caused by this pathology and other related diseases. These molecular targets have been gradually discovered and have essential roles in I-R resolution. Therefore, the current study is aimed at highlighting the importance of these discoveries. In this review, we inquire about the oxidative damage receptors that are relevant to reducing the damage induced by oxidative stress associated with I-R. Several complications on surgical techniques and pathology interventions do not mitigate the damage caused by I-R. Nevertheless, these therapies developed using alternative targets could work as coadjuvants in tissue transplants or I-R-related pathologies

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Long Noncoding RNA/Circular RNA-miRNA-mRNA Axes in Ischemia-Reperfusion Injury

Cited by 27 publications

References 150 publications

Suppression of circ_0008932 inhibits tumor growth and metastasis in osteosarcoma by targeting miR‑145‑5p

Suppression of circ_0008932 inhibits tumor growth and metastasis in osteosarcoma by targeting miR‑145‑5p

Comprehensive Analysis of Hub Genes Associated With Competing Endogenous RNA Networks in Stroke Using Bioinformatics Analysis

Therapeutic Targets for Regulating Oxidative Damage Induced by Ischemia-Reperfusion Injury: A Study from a Pharmacological Perspective

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