MiR-877-5p targets PDK-1 to promote aspirin-induced apoptosis in gastric mucosal cells.

细胞凋亡 流式细胞术 阿司匹林 基因敲除 转染 免疫印迹 下调和上调 小RNA 癌症研究 荧光素酶 化学 分子生物学 医学 生物 基因 生物化学
作者
Yuyu Lu,Shikun Zhang,Zhenyu Zhang,Zongdan Jiang,Wei‐Hao Sun
出处
期刊:PubMed 卷期号:76 (6): 256-260 被引量:1
标识
DOI:10.1691/ph.2021.0926
摘要

This study aimed to investigate the role of miR-877-5p in aspirin-induced gastric mucosal injury. MiRNA microarray analysis was performed using paired gastric mucosal samples to find differentially expressed miRNAs. miR-877-5p was selected for subsequent analyses. Used as a model system, gastric epithelial cells (GES-1) were transfected with miR-877-5p mimic/inhibitor, then treated with aspirin. The expression of miR-877-5p in GES-1 cells was examined using quantitative real-time PCR (qRT-PCR). Flow cytometry analysis was used to detect cell apoptosis. Western blot assay was used to measure the protein levels of PDK1. The interaction between miR-877-5p and PDK1 was determined by luciferase reporter assay. The expression of miR-877-5p in gastric mucosal injury samples was higher than that in normal samples. Also, depletion of miR-877-5p reduced the apoptosis of GES-1 cells. Luciferase reporting assay confirmed that PDK1 was a target gene of miR-877-5p. PDK1 inhibited the apoptosis of GES-1 cells treated by aspirin. Moreover, this inhibitory effect was abrogated after PDK1 knockdown. Downregulation of miR-877-5p reduced the apoptosis by targeting PDK1 in GES-1 cells treated by aspirin, indicating that miR-877-5p may be a potential therapeutic target for gastric mucosal injury caused by aspirin.

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