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Upregulated expression of long non-coding RNA MEG3 serves as a prognostic biomarker in severe pneumonia children and its regulatory mechanism

Severe pneumonia is a high-mortality disorder in children. The expression and underlying effects of lncRNA maternally expressed 3 (MEG3) were detected. The relationships between MEG3 and other parameters were reported by Pearson correlation. The prognostic importance of MEG3 was assessed by Kaplan-M...

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Autores principales: Guo, Jie, Zhang, Ning, Liu, Guozhi, Zhang, Aimei, Liu, Xin, Zheng, Jie
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Taylor & Francis 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8806474/
https://www.ncbi.nlm.nih.gov/pubmed/34558385
http://dx.doi.org/10.1080/21655979.2021.1979351
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author Guo, Jie
Zhang, Ning
Liu, Guozhi
Zhang, Aimei
Liu, Xin
Zheng, Jie
author_facet Guo, Jie
Zhang, Ning
Liu, Guozhi
Zhang, Aimei
Liu, Xin
Zheng, Jie
author_sort Guo, Jie
collection PubMed
description Severe pneumonia is a high-mortality disorder in children. The expression and underlying effects of lncRNA maternally expressed 3 (MEG3) were detected. The relationships between MEG3 and other parameters were reported by Pearson correlation. The prognostic importance of MEG3 was assessed by Kaplan-Meier (K-M) curve and COX analysis and its diagnostic potential was uncovered by the receiver operating characteristic (ROC) curve. Luciferase activity assay was performed to demonstrate the target gene of MEG3. Elevated expression of MEG3 and reduced microRNA-29 c (miR-29 c) were evaluated in severe pneumonia children, and a negative relationship between MEG3 and miR-29 c was propounded. MEG3 might function as an independent prognostic indicator. The diagnostic efficiency of MEG3 was also indicated for severe pneumonia children. In MRC-5 cell models and MH-S cell models, lipopolysaccharide (LPS) contributed to the increased expression of MEG3. Interference of MEG3 restricted the upregulation of MEG3 triggered by LPS. Silenced MEG3 protected MRC-5 and MH-S cells against damages managed by LPS on cell apoptosis, viability, and inflammation. MiR-29 c was a ceRNA of MEG3 and the absence of MEG3 abrogated the decreased expression of miR-29 c caused by LPS. Overall, the increased expression of MEG3 and the reduced levels of miR-29 c were identified in severe pneumonia. Prognostic and diagnostic significances of MEG3 provided a novel perspective for severe pneumonia. Disruption of MEG3 alleviated cell injury and inflammation as characterized by high LPS by binding miR-29 c.
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spelling pubmed-88064742022-02-02 Upregulated expression of long non-coding RNA MEG3 serves as a prognostic biomarker in severe pneumonia children and its regulatory mechanism Guo, Jie Zhang, Ning Liu, Guozhi Zhang, Aimei Liu, Xin Zheng, Jie Bioengineered Research Paper Severe pneumonia is a high-mortality disorder in children. The expression and underlying effects of lncRNA maternally expressed 3 (MEG3) were detected. The relationships between MEG3 and other parameters were reported by Pearson correlation. The prognostic importance of MEG3 was assessed by Kaplan-Meier (K-M) curve and COX analysis and its diagnostic potential was uncovered by the receiver operating characteristic (ROC) curve. Luciferase activity assay was performed to demonstrate the target gene of MEG3. Elevated expression of MEG3 and reduced microRNA-29 c (miR-29 c) were evaluated in severe pneumonia children, and a negative relationship between MEG3 and miR-29 c was propounded. MEG3 might function as an independent prognostic indicator. The diagnostic efficiency of MEG3 was also indicated for severe pneumonia children. In MRC-5 cell models and MH-S cell models, lipopolysaccharide (LPS) contributed to the increased expression of MEG3. Interference of MEG3 restricted the upregulation of MEG3 triggered by LPS. Silenced MEG3 protected MRC-5 and MH-S cells against damages managed by LPS on cell apoptosis, viability, and inflammation. MiR-29 c was a ceRNA of MEG3 and the absence of MEG3 abrogated the decreased expression of miR-29 c caused by LPS. Overall, the increased expression of MEG3 and the reduced levels of miR-29 c were identified in severe pneumonia. Prognostic and diagnostic significances of MEG3 provided a novel perspective for severe pneumonia. Disruption of MEG3 alleviated cell injury and inflammation as characterized by high LPS by binding miR-29 c. Taylor & Francis 2021-09-24 /pmc/articles/PMC8806474/ /pubmed/34558385 http://dx.doi.org/10.1080/21655979.2021.1979351 Text en © 2021 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group. https://creativecommons.org/licenses/by/4.0/This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) ), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Paper
Guo, Jie
Zhang, Ning
Liu, Guozhi
Zhang, Aimei
Liu, Xin
Zheng, Jie
Upregulated expression of long non-coding RNA MEG3 serves as a prognostic biomarker in severe pneumonia children and its regulatory mechanism
title Upregulated expression of long non-coding RNA MEG3 serves as a prognostic biomarker in severe pneumonia children and its regulatory mechanism
title_full Upregulated expression of long non-coding RNA MEG3 serves as a prognostic biomarker in severe pneumonia children and its regulatory mechanism
title_fullStr Upregulated expression of long non-coding RNA MEG3 serves as a prognostic biomarker in severe pneumonia children and its regulatory mechanism
title_full_unstemmed Upregulated expression of long non-coding RNA MEG3 serves as a prognostic biomarker in severe pneumonia children and its regulatory mechanism
title_short Upregulated expression of long non-coding RNA MEG3 serves as a prognostic biomarker in severe pneumonia children and its regulatory mechanism
title_sort upregulated expression of long non-coding rna meg3 serves as a prognostic biomarker in severe pneumonia children and its regulatory mechanism
topic Research Paper
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8806474/
https://www.ncbi.nlm.nih.gov/pubmed/34558385
http://dx.doi.org/10.1080/21655979.2021.1979351
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