Up-regulation of lncRNA WT1-AS ameliorates A β-stimulated neuronal injury through modulation of miR-186-5p/CCND2 axis in Alzheimer's disease

Cell Mol Biol (Noisy-le-grand). 2024 Jan 31;70(1):200-206. doi: 10.14715/cmb/2024.70.1.27.ABSTRACTAs a common neurodegenerative disorder, Alzheimer's disease (AD) seriously threatens human life. Long non-coding RNAs (lncRNAs) exhibit essential functions in AD development. Nevertheless, the detailed effects and possible mechanisms of lncRNA Wilms tumor 1 Antisense RNA (WT1-AS) in AD are largely unknown. In our studies, a total of 30 serum samples from AD patients were collected, and WT1-AS expressions were detected through qRT-PCR analysis. Additionally, an in vitro AD model was constructed by treating Aβ1-42 in human neuroblastoma cells. Functional assays were implemented to assess the impacts of WT1-AS on Aβ1-42-stimulated human neuroblastoma cell proliferation together with apoptosis. Moreover, relationship of WT1-AS, microRNA (miR)-186-5p as well as cyclin D2 (CCND2) could be predicted through bioinformatics tools as well as proved via dual-luciferase reporter experiments. Our results showed that WT1-AS together with CCND2 were low-expressed, while miR-186-5p presented high expression in AD serum samples together with Aβ1-42-stimulated human neuroblastoma cells. WT1-AS over-expression or miR-186-5p depletion notably promoted the proliferation, reduced the apoptosis, and decreased the p-Tau protein expressions of human neuroblastoma cells induced with Aβ1-42. Moreover, miR-186-5p combined with WT1-AS, and CCND2 was modulated by miR-186-5p. Furthermore, CCND2 elevation p...
Source: Cellular and Molecular Biology - Category: Molecular Biology Authors: Source Type: research