MicroRNA-107 Ameliorates Damage in a Cell Model of Alzheimer's Disease by Mediating the FGF7/FGFR2/PI3K/Akt Pathway.
Alzheimer's disease (AD), the most prevalent representation of dementia, is a neurodegenerative disease resulting from the degenerative disturbance of the central nervous system. Previous studies have indicated that miR-107 is reduced in the brain neocortex of patients with AD; however, its underlying mechanism is not clear. Therefore, the objective of this study was to explore the question of whether miR-107 participates in AD development. The study confirmed that the miR-107 expression levels were dramatically decreased in patients with AD and in beta-amyloid (Aβ) (Aβ)-treated SH-SY5Y cells compared with control groups. Upregulation of miR-107 reversed the inhibitory role of Aβ on cell proliferation and viability. In addition, miR-107 upregulation also ameliorated the Aβ-induced inflammation and apoptosis of SH-SY5Y cells. Furthermore, using bioinformatic prediction, dual-luciferase reporter assay (DLRA), quantitative polymerase chain reaction (qPCR), and Western blot (WB), miR-107 was confirmed to reduce the expression level of FGF7, and it subsequently deactivated the FGFR2/PI3K/Akt pathway. Moreover, FGF7 overexpression counteracted the role of miR-107 in the viability, proliferation, inflammation, and apoptosis of Aβ-induced SH-SY5Y cells.
['Chen|Wei|W|', 'Wu|Lin|L|', 'Hu|Yueqiang|Y|', 'Jiang|Lingfei|L|', 'Liang|Ni|N|', 'Chen|Jing|J|', 'Qin|Hongling|H|', 'Tang|Nong|N|http://orcid.org/0000-0001-8043-3743']
D000544:Alzheimer Disease D017209:Apoptosis D045744:Cell Line, Tumor D051523:Fibroblast Growth Factor 7 D006801:Humans D035683:MicroRNAs D019869:Phosphatidylinositol 3-Kinases D051057:Proto-Oncogene Proteins c-akt D051497:Receptor, Fibroblast Growth Factor, Type 2 D015398:Signal Transduction
FGF7 AD miR-107 Aβ Inflammation Apoptosis