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MiR-17-5p promotes cellular proliferation and invasiveness by targeting RUNX3 in gastric cancer

污渍 小RNA 细胞生长 生物 癌症研究 下调和上调 细胞凋亡 体内 分子生物学 癌症 逆转录聚合酶链式反应 信使核糖核酸 基因 生物化学 遗传学 生物技术
作者
Song Jin,Yingjun Liu,Tianyuan Wang,Bo Li,Shengsheng Zhang
出处
期刊:Biomedicine & Pharmacotherapy [Elsevier]
卷期号:128: 110246-110246 被引量:35
标识
DOI:10.1016/j.biopha.2020.110246
摘要

Dysregulated microRNAs (miRNAs/miRs) directly modulate the biological functions of gastric cancer (GC) cells and contribute to the initiation and progression of GC. MiR-17-5p and runt-related transcription factor 3 (RUNX3) have been reported to be related to GC progression; however, the specific interaction between miR-17-5p and RUNX3 in GC require further investigation. Western blotting, real-time PCR and immunohistochemistry were used to study the expression level of miR-17-5p and RUNX3 in gastric cancer tissues and plasma. The biological function of miR-17-5p was examined by measuring cell proliferation, apoptosis and cell invasion in vitro; the target gene of miR17-5p was identified by luciferase reporter assays, RNA Binding protein immunoprecipitation (RIP) and western blotting. In vivo animal study was conducted to confirm the role of miR-17-5p during tumorigensis of gastric cancer. This study showed that miR17-5p was upregulated in the plasma and tissues of patients with GC, while RUNX3 was downregulated in GC tissues. Functional experiments indicated that miR-17-5p mimics promoted the proliferation and invasion of GC via suppressing apoptosis in vitro. Furthermore, bioinformatics prediction, luciferase reporter assays, reverse transcription quantitative polymerase chain reaction assays, RIP and western blotting analysis demonstrated that RUNX3 was a direct target gene of miR-17-5p in GC. In addition, overexpression of RUNX3 suppressed the proliferation and invasiveness of GC cells. In vivo data indicated miR-17-5p agomir significantly promoted tumor growth. In contrast, miR-17-5p antagomir notably decreased tumor volume compared with control group. MiR-17-5p promoted the progression of GC via directly targeting RUNX3, suggesting that miR-17-5p and RUNX3 could be considered as diagnostic and therapeutic targets for patients with GC.
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