Research articles
ScienceAsia 49 (2023):ID 805-812 |doi:
10.2306/scienceasia1513-1874.2023.083
MiR-26a-5p promotes Alzheimer's disease by regulating
CDK5R1
Dujuan Caoa, Jing Shanga, Chongren Renb,*
ABSTRACT: Abnormal expression of miRNA is closely associated with disease, particularly Alzheimer?s disease (AD).
However, the function of miR-26a-5p in AD pathogenesis is not fully understood. Our aim was to investigate the
role of miR-26a-5p and its target gene CDK5R1 during the pathogenesis of AD. In this study, SH-SY5Y cells were
treated with beta-amyloid (A?) to create AD mimic cells and MiR-26a-5p, apoptotic biomarkers, and CDK5R1 were
evaluated by RT-qPCR. Transfection was performed to downregulate or upregulate miR-26a-5p and CDK5R1 and a
molecular correlation between CDK5R1 and miR-26a-5p was predicted using a luciferase reporter assay. Apoptotic
biomarkers and proteins associated with the Wnt/?-catenin signaling pathway in AD mimic cells were detected by
Western blotting and cell viability was examined using MTT. MiR-26a-5p levels were higher in the A?-coped SH-SY5Y
cell lines, which showed reduced viability compared to the control. This effect was reversed when miR-26a-5p was
knocked down. MiR-26a-5p has a binding site for CDK5R1, and overexpression of CDK5R1 enhanced cell viability and
increased Bcl-2 expression. Furthermore, CDK5R1 overexpression and miR-26a-5p downregulation positively regulated
the Wnt/?-catenin signaling pathway. The results showed that MiR-26a-5p is a critical pathogenic gene in AD and its
downregulation can be utilized as a novel therapeutic strategy for AD.
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| a |
Department of Neurology, Shanxi Bethune Hospital, Taiyuan 030012 China |
| b |
Department of General Surgery, Shanxi Bethune Hospital, Taiyuan 030012 China |
* Corresponding author, E-mail: renxiangxiang@126.com
Received 11 Feb 2023, Accepted 21 Aug 2023
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