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Long Non-Coding NONRATG001910.2 Promotes the Proliferation of Rat Mesangial Cell Line HBZY-1 Through the miR-339-3p/CTNNB1 Axis
Chronic glomerulonephritis (CGN) is one of the leading causes of end-stage renal disease (ESRD). A growing body of literature emphasizes the important role of long non-coding RNAs (lncRNAs) in the development and progression of the disease. However, the function of NONRATG001910.2 in the development...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Frontiers Media S.A.
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9096093/ https://www.ncbi.nlm.nih.gov/pubmed/35571052 http://dx.doi.org/10.3389/fgene.2022.834144 |
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author | Gao, Jiarong Zhu, Xiaoli Chen, Hao Jiang, Hui Shi, Miaomiao Wei, Liangbing Qin, Xiujuan |
author_facet | Gao, Jiarong Zhu, Xiaoli Chen, Hao Jiang, Hui Shi, Miaomiao Wei, Liangbing Qin, Xiujuan |
author_sort | Gao, Jiarong |
collection | PubMed |
description | Chronic glomerulonephritis (CGN) is one of the leading causes of end-stage renal disease (ESRD). A growing body of literature emphasizes the important role of long non-coding RNAs (lncRNAs) in the development and progression of the disease. However, the function of NONRATG001910.2 in the development of CGN was not well understood. This research aimed to investigate the effect of NONRATG001910.2 on CGN and revealed its potential molecular mechanisms. In this work, the expression of NONRATG001910.2 was detected by quantitative real-time polymerase chain reaction (qRT-RCR) in cell lines. We found that NONRATG001910.2 was significantly up-regulated in lipopolysaccharide (LPS) induced cells. High NONRATG001910.2 levels were associated with the development of CGN. In addition, NONRATG001910.2 knockdown inhibited cell proliferation and cell cycle. At the same time, we found that up-regulation of microRNA-339-3p (miR-339-3p) abrogated the biological roles of NONRATG001910.2 up-regulation. Moreover, the knockdown of CTNNB1 can upregulate miR-339-3p expression, thereby inhibiting cell proliferation. In conclusion, these results demonstrated that NONRATG001910.2 in LPS-stimulated rat mesangial cell line HBZY-1 (HBZY-1) by targeting miR-339-3p, which subsequently promotes the expression of CTNNB1, and suggested that NONRATG001910.2 may be a potential biomarker. |
format | Online Article Text |
id | pubmed-9096093 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-90960932022-05-13 Long Non-Coding NONRATG001910.2 Promotes the Proliferation of Rat Mesangial Cell Line HBZY-1 Through the miR-339-3p/CTNNB1 Axis Gao, Jiarong Zhu, Xiaoli Chen, Hao Jiang, Hui Shi, Miaomiao Wei, Liangbing Qin, Xiujuan Front Genet Genetics Chronic glomerulonephritis (CGN) is one of the leading causes of end-stage renal disease (ESRD). A growing body of literature emphasizes the important role of long non-coding RNAs (lncRNAs) in the development and progression of the disease. However, the function of NONRATG001910.2 in the development of CGN was not well understood. This research aimed to investigate the effect of NONRATG001910.2 on CGN and revealed its potential molecular mechanisms. In this work, the expression of NONRATG001910.2 was detected by quantitative real-time polymerase chain reaction (qRT-RCR) in cell lines. We found that NONRATG001910.2 was significantly up-regulated in lipopolysaccharide (LPS) induced cells. High NONRATG001910.2 levels were associated with the development of CGN. In addition, NONRATG001910.2 knockdown inhibited cell proliferation and cell cycle. At the same time, we found that up-regulation of microRNA-339-3p (miR-339-3p) abrogated the biological roles of NONRATG001910.2 up-regulation. Moreover, the knockdown of CTNNB1 can upregulate miR-339-3p expression, thereby inhibiting cell proliferation. In conclusion, these results demonstrated that NONRATG001910.2 in LPS-stimulated rat mesangial cell line HBZY-1 (HBZY-1) by targeting miR-339-3p, which subsequently promotes the expression of CTNNB1, and suggested that NONRATG001910.2 may be a potential biomarker. Frontiers Media S.A. 2022-04-28 /pmc/articles/PMC9096093/ /pubmed/35571052 http://dx.doi.org/10.3389/fgene.2022.834144 Text en Copyright © 2022 Gao, Zhu, Chen, Jiang, Shi, Wei and Qin. https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. |
spellingShingle | Genetics Gao, Jiarong Zhu, Xiaoli Chen, Hao Jiang, Hui Shi, Miaomiao Wei, Liangbing Qin, Xiujuan Long Non-Coding NONRATG001910.2 Promotes the Proliferation of Rat Mesangial Cell Line HBZY-1 Through the miR-339-3p/CTNNB1 Axis |
title | Long Non-Coding NONRATG001910.2 Promotes the Proliferation of Rat Mesangial Cell Line HBZY-1 Through the miR-339-3p/CTNNB1 Axis |
title_full | Long Non-Coding NONRATG001910.2 Promotes the Proliferation of Rat Mesangial Cell Line HBZY-1 Through the miR-339-3p/CTNNB1 Axis |
title_fullStr | Long Non-Coding NONRATG001910.2 Promotes the Proliferation of Rat Mesangial Cell Line HBZY-1 Through the miR-339-3p/CTNNB1 Axis |
title_full_unstemmed | Long Non-Coding NONRATG001910.2 Promotes the Proliferation of Rat Mesangial Cell Line HBZY-1 Through the miR-339-3p/CTNNB1 Axis |
title_short | Long Non-Coding NONRATG001910.2 Promotes the Proliferation of Rat Mesangial Cell Line HBZY-1 Through the miR-339-3p/CTNNB1 Axis |
title_sort | long non-coding nonratg001910.2 promotes the proliferation of rat mesangial cell line hbzy-1 through the mir-339-3p/ctnnb1 axis |
topic | Genetics |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9096093/ https://www.ncbi.nlm.nih.gov/pubmed/35571052 http://dx.doi.org/10.3389/fgene.2022.834144 |
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