ArticleBioscience reports2020
Knockdown of long non-coding RNA SOX21-AS1 attenuates amyloid-β-induced neuronal damage by sponging miR-107.
Article in Bioscience reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 39 citations in OpenAlex.
- lncRNAs: key player in Aβ deposition.RNA biology · 2026Review
- STZ‑induced sporadic Alzheimer's in rats: behavioral, histopathological, and MiRNA profiles.Journal of molecular histology · 2026Article
- miR-196a reduces mutant Huntingtin aggregates by Rad23b-mediated degradation in Huntington's disease.Journal of biomedical science · 2026Article
- Pivotal Role of miRNA-lncRNA Interactions in Human Diseases.Molecular biotechnology · 2025Review
- Regulatory role of LncRNA FMR1-AS1 in the pathogenesis of alzheimer's disease based on bioinformatics and in vitro experimental validation.Scientific reports · 2025Article
- Exosomes and non-coding RNAs: bridging the gap in Alzheimer's pathogenesis and therapeutics.Metabolic brain disease · 2025Review
- The Role of circRNAs in the Pathological Mechanisms of Alzheimer's Disease: Potential Biomarkers for Diagnosis.Current neuropharmacology · 2025Review
- The Role of Non-Coding RNAs in Mitochondrial Dysfunction of Alzheimer's Disease.Journal of molecular neuroscience : MN · 2024Review
- Exploring the Frontier: Antisense Long Non-Coding RNAs as Key Regulators in Alzheimer's Disease.Aging and disease · 2024Review
- Role of Epigenetic Modulation in Neurodegenerative Diseases: Implications of Phytochemical Interventions.Antioxidants (Basel, Switzerland) · 2024Review
- NcRNAs: A synergistically antiapoptosis therapeutic tool in Alzheimer's disease.CNS neuroscience & therapeutics · 2024Review
- Role of long non-coding RNAs in the pathophysiology of Alzheimer's disease and other dementias.Molecular biology reports · 2024Review
- Long-noncoding RNAs as epigenetic regulators in neurodegenerative diseases.Neural regeneration research · 2023Review
- MicroRNAs: protective regulators for neuron growth and development.Neural regeneration research · 2023Review
- SRY-box transcription factor 21 antisense divergent transcript 1: Regulatory roles and clinical significance in neoplastic conditions and Alzheimer's Disease.Journal of Cancer · 2023Review
- New Insights into lncRNAs in Aβ Cascade Hypothesis of Alzheimer's Disease.Biomolecules · 2022Review
- Epigenetic Changes in Prion and Prion-like Neurodegenerative Diseases: Recent Advances, Potential as Biomarkers, and Future Perspectives.International journal of molecular sciences · 2022Review
- Review
- miR-212-3p attenuates neuroinflammation of rats with Alzheimer's disease via regulating the SP1/BACE1/NLRP3/Caspase-1 signaling pathway.Bosnian journal of basic medical sciences · 2022Article
- Expression of Linear and Circular lncRNAs in Alzheimer's Disease.Journal of molecular neuroscience : MN · 2022Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAlzheimer'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.
methodsTo construct the AD model, SH-SY5Y and SK-N-SH cells were treated with amyloid-β1-42 (Aβ1-42). 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.
resultsSOX21-AS1 expression was augmented while miR-107 expression was decreased in Aβ1-42-treated SH-SY5Y and SK-N-SH cells. Moreover, Aβ1-42 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 Aβ1-42 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 Aβ1-42-treated SH-SY5Y and SK-N-SH cells mediated by miR-107 inhibition were partly recovered by SOX21-AS1 depletion.
conclusionSOX21-AS1 silencing could attenuate Aβ1-42-induced neuronal damage by sponging miR-107, which provided a possible strategy for the treatment of AD.
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