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Knockdown of long non-coding RNA SOX21-AS1 attenuates amyloid-β-induced neuronal damage by sponging miR-107

Background: Alzheimer’s disease (AD), which has no effective drugs to delay or prevent its progression, is a multifactorial complex neurodegenerative disease. Long non-coding RNA SOX21 antisense RNA1 (SOX21-AS1) is associated with the development of AD, but the underlying molecular mechanism of SOX2...

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Autores principales: Xu, Wanru, Li, Kai, Fan, Qian, Zong, Biyun, Han, Ling
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Portland Press Ltd. 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7103586/
https://www.ncbi.nlm.nih.gov/pubmed/32124921
http://dx.doi.org/10.1042/BSR20194295
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author Xu, Wanru
Li, Kai
Fan, Qian
Zong, Biyun
Han, Ling
author_facet Xu, Wanru
Li, Kai
Fan, Qian
Zong, Biyun
Han, Ling
author_sort Xu, Wanru
collection PubMed
description Background: Alzheimer’s disease (AD), which has no effective drugs to delay or prevent its progression, is a multifactorial complex neurodegenerative disease. Long non-coding RNA SOX21 antisense RNA1 (SOX21-AS1) is associated with the development of AD, but the underlying molecular mechanism of SOX21-AS1 in AD is still largely unclear. Methods: To construct the AD model, SH-SY5Y and SK-N-SH cells were treated with amyloid-β(1-42) (Aβ(1-42)). Quantitative real-time polymerase chain reaction (qRT-PCR) was executed to detect the expression of SOX21-AS1 and miRNA-107. Western blot analysis was utilized to assess the levels of phosphorylated Tau (p-Tau). 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) or flow cytometry assay was employed to determine the viability and apoptosis of SH-SY5Y and SK-N-SH cells. The relationship between SOX21-AS1 and miRNA-107 was verified with the dual-luciferase reporter assay. Results: SOX21-AS1 expression was augmented while miR-107 expression was decreased in Aβ(1-42)-treated SH-SY5Y and SK-N-SH cells. Moreover, Aβ(1-42) elevated the levels of p-Tau and impeded viability and induced apoptosis of SH-SY5Y and SK-N-SH cells. Also, SOX21-AS1 silencing attenuated Aβ(1-42) mediated the levels of p-Tau, viability, and apoptosis of SH-SY5Y and SK-N-SH cells. Importantly, SOX21-AS1 acted as a sponge for miR-107 in SH-SY5Y and SK-N-SH cells. Furthermore, the increase in p-Tau levels and apoptosis and the repression of viability of Aβ(1-42)-treated SH-SY5Y and SK-N-SH cells mediated by miR-107 inhibition were partly recovered by SOX21-AS1 depletion. Conclusion: SOX21-AS1 silencing could attenuate Aβ(1-42)-induced neuronal damage by sponging miR-107, which provided a possible strategy for the treatment of AD.
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spelling pubmed-71035862020-04-06 Knockdown of long non-coding RNA SOX21-AS1 attenuates amyloid-β-induced neuronal damage by sponging miR-107 Xu, Wanru Li, Kai Fan, Qian Zong, Biyun Han, Ling Biosci Rep Cell Cycle, Growth & Proliferation Background: Alzheimer’s disease (AD), which has no effective drugs to delay or prevent its progression, is a multifactorial complex neurodegenerative disease. Long non-coding RNA SOX21 antisense RNA1 (SOX21-AS1) is associated with the development of AD, but the underlying molecular mechanism of SOX21-AS1 in AD is still largely unclear. Methods: To construct the AD model, SH-SY5Y and SK-N-SH cells were treated with amyloid-β(1-42) (Aβ(1-42)). Quantitative real-time polymerase chain reaction (qRT-PCR) was executed to detect the expression of SOX21-AS1 and miRNA-107. Western blot analysis was utilized to assess the levels of phosphorylated Tau (p-Tau). 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) or flow cytometry assay was employed to determine the viability and apoptosis of SH-SY5Y and SK-N-SH cells. The relationship between SOX21-AS1 and miRNA-107 was verified with the dual-luciferase reporter assay. Results: SOX21-AS1 expression was augmented while miR-107 expression was decreased in Aβ(1-42)-treated SH-SY5Y and SK-N-SH cells. Moreover, Aβ(1-42) elevated the levels of p-Tau and impeded viability and induced apoptosis of SH-SY5Y and SK-N-SH cells. Also, SOX21-AS1 silencing attenuated Aβ(1-42) mediated the levels of p-Tau, viability, and apoptosis of SH-SY5Y and SK-N-SH cells. Importantly, SOX21-AS1 acted as a sponge for miR-107 in SH-SY5Y and SK-N-SH cells. Furthermore, the increase in p-Tau levels and apoptosis and the repression of viability of Aβ(1-42)-treated SH-SY5Y and SK-N-SH cells mediated by miR-107 inhibition were partly recovered by SOX21-AS1 depletion. Conclusion: SOX21-AS1 silencing could attenuate Aβ(1-42)-induced neuronal damage by sponging miR-107, which provided a possible strategy for the treatment of AD. Portland Press Ltd. 2020-03-27 /pmc/articles/PMC7103586/ /pubmed/32124921 http://dx.doi.org/10.1042/BSR20194295 Text en © 2020 The Author(s). https://creativecommons.org/licenses/by/4.0/ This is an open access article published by Portland Press Limited on behalf of the Biochemical Society and distributed under the Creative Commons Attribution License 4.0 (CC BY).
spellingShingle Cell Cycle, Growth & Proliferation
Xu, Wanru
Li, Kai
Fan, Qian
Zong, Biyun
Han, Ling
Knockdown of long non-coding RNA SOX21-AS1 attenuates amyloid-β-induced neuronal damage by sponging miR-107
title Knockdown of long non-coding RNA SOX21-AS1 attenuates amyloid-β-induced neuronal damage by sponging miR-107
title_full Knockdown of long non-coding RNA SOX21-AS1 attenuates amyloid-β-induced neuronal damage by sponging miR-107
title_fullStr Knockdown of long non-coding RNA SOX21-AS1 attenuates amyloid-β-induced neuronal damage by sponging miR-107
title_full_unstemmed Knockdown of long non-coding RNA SOX21-AS1 attenuates amyloid-β-induced neuronal damage by sponging miR-107
title_short Knockdown of long non-coding RNA SOX21-AS1 attenuates amyloid-β-induced neuronal damage by sponging miR-107
title_sort knockdown of long non-coding rna sox21-as1 attenuates amyloid-β-induced neuronal damage by sponging mir-107
topic Cell Cycle, Growth & Proliferation
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7103586/
https://www.ncbi.nlm.nih.gov/pubmed/32124921
http://dx.doi.org/10.1042/BSR20194295
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