LncRNA H19 promotes keloid formation through targeting the miR-769-5p/EIF3A pathway

Xu, Lin-gang; Sun, Nan; Li, Guangshuai; Linbo, Liu

doi:10.1007/s11010-020-04024-x

Cited by 15 publications

(17 citation statements)

References 32 publications

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“…A previous study suggested that the abundance of H19 in keloid tissue and fibroblasts was significantly increased, and its downregulation inhibited cell proliferation [ 11 ]. Xu et al [ 10 ] have shown that downregulation of H19 expression inhibits the aberrant proliferation and ECM deposition of keloid fibroblasts and promotes apoptosis. Wang et al [ 9 ] collected 80 keloid tissues and isolated fibroblasts and found that PCDNA3.1-H19 could enhance the viability, proliferation, migration, and invasion of fibroblasts, whereas silencing H19 significantly inhibited the metastasis and proliferation of fibroblasts.…”

Section: Discussionmentioning

confidence: 99%

RETRACTED ARTICLE: Long non-coding RNA H19 aggravates keloid progression by upregulating SMAD family member 5 expression via miR-196b-5p

Chen

Wei

2022

Bioengineered

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Accumulating evidence suggests that long non-coding RNAs (lncRNAs) participate in the formation and development of keloids, a benign tumor. In addition, lncRNA H19 has been shown to act on the biological processes of keloids. This study aimed to identify other important mechanisms of the effect of lncRNA H19 on keloid formation. The H19, miR-196b-5p, and SMAD family member 5 (SMAD5) expression levels were detected using quantitative reverse transcriptase polymerase chain reaction (qRT-PCR) and Western blotting. Subcellular localization of lncRNA H19 was detected using a nuclear–cytoplasmic separation assay. Cell viability and proliferation were measured using counting kit-8 and colony formation assays. Bax and Bcl-2 levels were examined using Western blot analysis. The interaction between H19 and miR-196b-5p or SMAD5 was verified using a dual-luciferase reporter assay. H19 and SMAD5 expression was upregulated in keloid tissue and fibroblasts, whereas miR-196b-5p expression was downregulated. Knockdown of H19, overexpression of miR-196b-5p, or knockdown of SMAD5 inhibited the viability and proliferation of keloid fibroblasts and promoted apoptosis. Overexpression of H19 or SMAD5 and knockdown of miR-196b-5p promoted viability and proliferation and inhibited apoptosis. miR-196b-5p was identified as a H19 sponge, and SMAD5 was identified as a miR-196b-5p target. The combination of lncRNA H19 and miR-196b-5p regulates SMAD5 expression and promotes keloid formation, thus providing a new direction for keloid treatment.

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Section: Discussionmentioning

confidence: 99%

RETRACTED ARTICLE: Long non-coding RNA H19 aggravates keloid progression by upregulating SMAD family member 5 expression via miR-196b-5p

Chen

Wei

2022

Bioengineered

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“…The lack of alveolar surface-active substances increases the surface tension of the alveoli and decreases compliance. Furthermore, overexpression of miR-769-5p inhibits the proliferation, migration, and invasion and promotes the apoptosis of keloid fibroblasts [ 39 , 40 ]. miR-769-5p may inhibit fibrosis during BPD development, thus exerting a protective effect.…”

Section: Discussionmentioning

confidence: 99%

Functional Analysis of Bronchopulmonary Dysplasia-Related Neuropeptides in Preterm Infants and miRNA-Based Diagnostic Model Construction

Zhang¹,

Kong

Zhang³

et al. 2022

Computational and Mathematical Methods in Medicine

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Background. Bronchopulmonary dysplasia (BPD) has a high mortality rate. This study was aimed at identifying and analysing the risk factors associated with BPD using bioinformatic and mechanical analyses and establishing a predictive model to assess the risk of BPD in preterm infants. Methods. We identified differentially expressed RNAs via the intersection of miRNAs between datasets. Online analysis tools were used to predict genes targeted by differentially expressed miRNAs (DEmiRNAs) and to generate and visualise competing endogenous RNA (ceRNA) coexpression networks. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses were subsequently performed on the DEmiRNAs. In addition, an intersection analysis was performed on mRNA and neuropeptide-related genes in the ceRNA network. DEmiRNAs associated with BPD and those involved in ceRNA networks were used to establish a diagnostic prediction model. The GSE108604 dataset was used as a validation set to verify the model. Results. A total of 26 DEmiRNAs were identified from the tracheal aspirates (TAs) of patients with BPD and healthy controls. In addition, a total of 1076 DEmRNAs were obtained from the GSE8586 dataset. Functional enrichment analysis of DEmRNAs revealed an abnormal reduction in mitochondrial-related activity and cellular responses to oxidative stress in patients with BPD. The neuropeptide-related genes OPRL1 and NPPA were found to be upregulated in BPD samples. Eventually, hsa-miR-1258, hsa-miR-298, hsa-miR-483-3p, and hsa-miR-769-5p were screened out and used to establish the prediction model. Calibration curves and detrended correspondence analysis (DCA) revealed that the model had good clinical applicability. Conclusions. The prediction model provided a simple method for individualised assessment, early diagnosis, and prevention of BPD risk in preterm infants.

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“…lncRNA DLEU2, lncRNA H19 and lncRNA LINC01116 have been described to act as specific miRNA sponges ( Table 4 ), promoting the proliferation of fibroblasts and enhancing cell migration [ 136 , 162 , 163 ]. lncRNA LINC00937 hinders cell proliferation by the miR-28-5p/MC1R axis in keloids, and its expression is inhibited in fibroblasts [ 164 ].…”

Section: Reviewmentioning

confidence: 99%

Advances in the pathogenesis and clinical application prospects of tumor biomolecules in keloid

et al. 2022

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Keloid scarring is a kind of pathological healing manifestation after skin injury and possesses various tumor properties, such as the Warburg effect, epithelial–mesenchymal transition (EMT), expression imbalances of apoptosis-related genes and the presence of stem cells. Abnormal expression of tumor signatures is critical to the initiation and operation of these effects. Although previous experimental studies have recognized the potential value of a single or several tumor biomolecules in keloids, a comprehensive evaluation system for multiple tumor signatures in keloid scarring is still lacking. This paper aims to summarize tumor biomolecules in keloids from the perspectives of liquid biopsy, genetics, proteomics and epigenetics and to investigate their mechanisms of action and feasibility from bench to bedside. Liquid biopsy is suitable for the early screening of people with keloids due to its noninvasive and accurate performance. Epigenetic biomarkers do not require changes in the gene sequence and their reversibility and tissue specificity make them ideal therapeutic targets. Nonetheless, given the ethnic specificity and genetic predisposition of keloids, more large-sample multicenter studies are indispensable for determining the prevalence of these signatures and for establishing diagnostic criteria and therapeutic efficacy estimations based on these molecules.

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LncRNA H19 promotes keloid formation through targeting the miR-769-5p/EIF3A pathway

Cited by 15 publications

References 32 publications

RETRACTED ARTICLE: Long non-coding RNA H19 aggravates keloid progression by upregulating SMAD family member 5 expression via miR-196b-5p

RETRACTED ARTICLE: Long non-coding RNA H19 aggravates keloid progression by upregulating SMAD family member 5 expression via miR-196b-5p

Functional Analysis of Bronchopulmonary Dysplasia-Related Neuropeptides in Preterm Infants and miRNA-Based Diagnostic Model Construction

Advances in the pathogenesis and clinical application prospects of tumor biomolecules in keloid

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