Long Noncoding RNA EBF3-AS Promotes Neuron Apoptosis in Alzheimer's Disease

Gu, Cheng; Chen, Cheng; Wu, Ruipeng; Tong, Dong; Hu, Xiaojuan; Yao, Yuping; Zhang, Yi

doi:10.1089/dna.2017.4012

Cited by 85 publications

(50 citation statements)

References 20 publications

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“…Zhao et al disclosed that lncRNA NEAT1 promoted the progression of AD by modulating the miR-124/BACE1 axis [23]. Also, reduced lncRNA EBF3-AS expression could overturn Aβ-induced apoptosis of SH-SY5Y cells [24]. In the present study, Aβ could enhance p-Tau protein level, repressed viability and promoted apoptosis of SH-SY5Y and SK-N-SH cells.…”

Section: Discussionsupporting

confidence: 54%

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

Fan

et al. 2020

Bioscience Reports

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Correspondence: Ling Han (shuixiebu997@126.com) 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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Section: Discussionsupporting

confidence: 54%

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

Fan

et al. 2020

Bioscience Reports

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“…Antisense transcript of EBF3 (EBF3-AS) reduces early B cell factor 3 (EBF3) mRNA expression and promotes cell death. In an AD mouse model and Aβ-treated cells, EBF3-AS upregulation was found to promote apoptosis [97,103]. NAT-RAd18 is an antisense transcript of RAd18.…”

Section: Ncrnas In the Regulation Of Ad-associated Apoptosismentioning

confidence: 99%

Functional roles and networks of non-coding RNAs in the pathogenesis of neurodegenerative diseases

2020

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Recent transcriptome analyses have revealed that noncoding RNAs (ncRNAs) are broadly expressed in mammalian cells and abundant in the CNS, with tissue and cell type-specific expression patterns. Moreover, ncRNAs have been found to intricately and dynamically regulate various signaling pathways in neurodegeneration. As such, some antisense transcripts and microRNAs are known to directly affect neurodegeneration in disease contexts. The functions of ncRNAs in pathogenesis are unique for each disorder, as are the pertinent networks of ncRNA/miRNA/ mRNA that mediate these functions. Thus, further understanding of ncRNA biogenesis and effects might aid the discovery of diagnostic biomarkers or development of effective therapeutics for neurodegenerative disorders. Here, we review the ncRNAs that have so far been identified in major neurodegenerative disease etiology and the mechanisms that link ncRNAs with disease-specific phenotypes, such as HTT aggregation in HD, α-synuclein in PD, and Aβ plaques and hyperphosphorylated Tau in AD. We also summarize the known lncRNA/miRNA/mRNA networks that participate in neurodegenerative diseases, and we discuss ncRNA-related treatments shown to delay disease onset and prolong lifespan in rodent models.

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“…BC1, another type of lncRNA, is found to induce APP mRNA translation via association with fragile X syndrome protein (FMRP) in mouse model AD brains ( Zhang T. et al, 2017 ). It was recently reported that EBF3 knockdown can reverse Aβ25-35-induced apoptosis in SH-SY5Y cells, and that lncRNA EBF3-AS promotes neuron apoptosis in AD through regulation of EBF3 expression ( Gu et al, 2018 ). Furthermore, the overexpression of Aβ and Aβ-42 in AD could increase BACE1 antisense transcript lncRNA levels, leading to amyloid protein aggregation ( Faghihi et al, 2008 ).…”

Section: Long Non-coding Rnas In Admentioning

confidence: 99%

The Epigenetics of Alzheimer’s Disease: Factors and Therapeutic Implications

2018

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Alzheimer’s disease (AD) is a well-known neurodegenerative disorder that imposes a great burden on the world. The mechanisms of AD are not yet fully understood. Current insight into the role of epigenetics in the mechanism of AD focuses on DNA methylation, remodeling of chromatin, histone modifications and non-coding RNA regulation. This review summarizes the current state of knowledge regarding the role of epigenetics in AD and the possibilities for epigenetically based therapeutics. The general conclusion is that epigenetic mechanisms play a variety of crucial roles in the development of AD, and there are a number of viable possibilities for treatments based on modulating these effects, but significant advances in knowledge and technology will be needed to move these treatments from the bench to the bedside.

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Long Noncoding RNA EBF3-AS Promotes Neuron Apoptosis in Alzheimer's Disease

Cited by 85 publications

References 20 publications

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

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

Functional roles and networks of non-coding RNAs in the pathogenesis of neurodegenerative diseases

The Epigenetics of Alzheimer’s Disease: Factors and Therapeutic Implications

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