支票2
细胞凋亡
DNA损伤
细胞生物学
检查点激酶2
细胞
癌症研究
程序性细胞死亡
化学
生物
基因
细胞周期检查点
DNA
细胞周期
遗传学
突变
种系突变
作者
A Mula,Binbin Yan,Bingcheng Hu,Yue Su,Xuesong Yuan
出处
期刊:Cellular and Molecular Biology
日期:2023-09-30
卷期号:69 (9): 118-124
标识
DOI:10.14715/cmb/2023.69.9.17
摘要
DNA damage of neurons is accumulated in Alzheimer's disease (AD). DNA damage-activated Checkpoint kinase 2 (CHEK2) is evaluated in Aβ-treated Neuro2a APPSwe/Δ9 cells, and the miR-669b-5p was specifically down-regulated. However, the underlying molecular mechanism between CHEK2 and miR-669b-5p in Neuro2a APPSwe/Δ9 cells remains unclear. This research discovers that in A-treated Neuro2a APPSwe/Δ9 cells, CHEK2 expression and miR-669b-5p expression were inversely correlated. In addition, miR-669b-5p mimics increased cell survival and proliferation in Neuro2a APPSwe/Δ9 cells while decreasing the production of inflammatory cytokines and cell death. Furthermore, it is observed that CHEK2 was a miR-669b-5p downstream target gene and that CHEK2 restored the miR-669b-5p's functions. According to this research, miR-669b-5p is a potential therapy for Alzheimer's patients since it slows the advancement of the disease.
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