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MicroRNA-138 promotes neuroblastoma SH-SY5Y cell apoptosis by directly targeting DEK in Alzheimer’s disease cell model

Authors
  • Miao, Jin1, 2
  • Jing, Jin2
  • Shao, Yixiang2
  • Sun, Huaichang1
  • 1 Yangzhou University, Yangzhou, Jiangsu, 225009, People’s Republic of China , Yangzhou (China)
  • 2 Nantong University, Nantong, Jiangsu, 226000, People’s Republic of China , Nantong (China)
Type
Published Article
Journal
BMC Neuroscience
Publisher
Springer (Biomed Central Ltd.)
Publication Date
Jul 31, 2020
Volume
21
Issue
1
Identifiers
DOI: 10.1186/s12868-020-00579-z
Source
Springer Nature
Keywords
License
Green

Abstract

BackgroundAlzheimer’s disease (AD) is a progressive neuro-degenerative disease with a major manifestation of dementia. MicroRNAs were reported to regulate the transcript expression in patients with Alzheimer’s disease (AD). In this study, we investigated the roles of miR-138, a brain-enriched miRNA, in the AD cell model.MethodsThe targets of miRNA-138 was predicted by bioinformatic analysis. The expression levels of DEK at both mRNA and protein levels were determined by qRT-PCR and Western blot, respectively. Luciferase assays were carried out to examine cell viabilities. Hoechst 33258 staining was used to detect cell apoptosis.ResultsOur results demonstrated that the expression levels of miR-138 were increased in AD model, and DEK was a target of miR-138. Overexpression of miR-138 in SH-SY5Y cells obviously down-regulated the expression of DEK in SH-SY5Y cells, resulting in the inactivation of AKT and increased expression levels of proapoptotic caspase-3. MiR-138 mediated-suppression of DEK increased the susceptibility of cell apoptosis.ConclusionsMicroRNA-138 promotes cell apoptosis of SH-SY5Y by targeting DEK in SH-SY5Y AD cell model. The regulation of miR-138 may contribute to AD via down-regulation of the DEK/AKT pathway.

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