ZBTB20-AS1 promoted Alzheimer's disease progression through ZBTB20/GSK-3β/Tau pathway
To elucidate the potential molecular mechanisms of ZBTB20-AS1 on ZBTB20 and GSK-3β/Tau signaling pathway in the pathogenesis of Alzheimer's disease (AD), SH-SY5Y cells were obtained for in vitro experiments and AD models were constructed using β-Amyloid 1–42. CCK8 assay was implemented for dete...
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Published in | Biochemical and biophysical research communications Vol. 640; pp. 88 - 96 |
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Main Authors | , , , , |
Format | Journal Article |
Language | English |
Published |
United States
Elsevier Inc
15.01.2023
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Subjects | |
Online Access | Get full text |
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Summary: | To elucidate the potential molecular mechanisms of ZBTB20-AS1 on ZBTB20 and GSK-3β/Tau signaling pathway in the pathogenesis of Alzheimer's disease (AD), SH-SY5Y cells were obtained for in vitro experiments and AD models were constructed using β-Amyloid 1–42. CCK8 assay was implemented for determining cell viability. Flow cytometry was used for cell apoptosis detection. Dual-luciferase reporter and RNA-RNA pull down assay was employed for elucidating molecular interactions. Immunohistochemistry, RT-qPCR and western blotting were performed for measuring gene expression. The results showed that expression of LncRNA ZBTB20-AS1 was significantly upregulated, while ZBTB20 was downregulated in SH-SY5Y-AD cells. ZBTB20 was the target gene of LncRNA ZBTB20-AS1. Overexpression of ZBTB20 or knockdown of LncRNA ZBTB20-AS1 inhibited SH-SY5Y-AD cells apoptosis and suppressed GSK3β/Tau pathway, and knockdown of ZBTB20-AS1 increased cell viability and decreased apoptosis. In conclusion, overexpression of ZBTB20-AS1 inhibited ZBTB20 expression and promoted GSK-3β expression and Tau phosphorylation, contributing to the development of AD.
•LncRNA ZBTB20-AS1 was upregulated in AD.•miR-132–3p was the target gene of LncRNA ZBTB20-AS1.•ZBTB20 inhibited AD cells apoptosis and suppressed GSK3β/Tau pathway.•Knockdown of LncRNA ZBTB20-AS1 alleviated the progression of AD. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0006-291X 1090-2104 |
DOI: | 10.1016/j.bbrc.2022.11.107 |