Circular RNA HIPK3 promotes glioma progression by binding to miR-124-3p

基因敲除 胶质瘤 生物 流式细胞术 报告基因 转染 细胞凋亡 车站3 细胞生长 细胞周期 癌症研究 细胞培养 基因表达 分子生物学 基因 遗传学
作者
Daling Hu,Yin Zhang
出处
期刊:Gene [Elsevier BV]
卷期号:690: 81-89 被引量:66
标识
DOI:10.1016/j.gene.2018.11.073
摘要

This study aims to investigate whether circ-HIPK3 could promote the proliferation and invasion of glioma cells by upregulating STAT3 after binding to miR-124-3p, thus participating in the development of glioma. Expression levels of circ-HIPK3, miR-124-3p and STAT3 in glioma cell lines were determined using qRT-PCR. The regulatory effects of circ-HIPK3, miR-124-3p and STAT3 on proliferative and invasive capacities of glioma cells were accessed using EdU assay, CCK-8 assay and invasion assay, respectively. Cell cycle assay and cell apoptosis assay were performed by flow cytometry. Dual-luciferase reporter gene assay was conducted to determine the binding condition among circ-HIPK3, miR-124-3p and STAT3. Rescue experiments were performed in co-transfected glioma cells. QRT-PCR data showed that circ-HIPK3 and STAT3 are highly expressed, whereas miR-124-3p is lowly expressed in glioma cells than those of negative control cell. Knockdown of circ-HIPK3 in U87 and U251 cells inhibited their proliferative and invasive capacities. On the contrary, miR-124-3p knockdown improved proliferative and migratory capacities. Dual-luciferase reporter gene assay exerted that circ-HIPK3 could bind to miR-124-3p and STAT3 is the target gene of miR-124-3p. Western blot results elucidated that circ-HIPK3 stabilizes STAT3 expression, whereas miR-124-3p degrades STAT3 expression. Rescue experiments demonstrated that overexpression of circ-HIPK3 could partially reverse the inhibited proliferative and migratory capacities induced by miR-124-3p in U87 and U251 cells. In summary, we found that overexpression of circ-HIPK3 promotes proliferative and invasive capacities of glioma cells by sponging miR-124-3p to upregulate STAT3 expression.

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