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首页> 外文期刊>Cellular Physiology and Biochemistry >Kaiso (ZBTB33) Downregulation by Mirna-181a Inhibits Cell Proliferation, Invasion, and the Epithelial–Mesenchymal Transition in Glioma Cells
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Kaiso (ZBTB33) Downregulation by Mirna-181a Inhibits Cell Proliferation, Invasion, and the Epithelial–Mesenchymal Transition in Glioma Cells

机译:Kaiso(ZBTB33)下调的Mirna-181a抑制胶质瘤细胞的增殖,侵袭和上皮-间质转化

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Background/Aims Kaiso (ZBTB33) expression is closely associated with the progression of many cancers and microRNA (miRNA) processing. MiR-181a plays critical roles in multiple cancers; however, its precise mechanisms in glioma have not been well clarified. The goal of this study was to evaluate the interaction between Kaiso and miR-181a in glioma. Methods Quantitative real-time PCR (qRT-PCR) was performed to detect the levels of Kaiso and miR-181a in glioma tissues and cell lines. Cell proliferation, invasion, and the epithelial–mesenchymal transition (EMT) were evaluated to analyze the biological functions of miR-181a and Kaiso in glioma cells. The mRNA and protein levels of Kaiso were measured by qRT-PCR and western blotting, respectively. Meanwhile, luciferase assays were performed to validate Kaiso as a miR-181a target in glioma cells. Results We found that the level of miR-181a was the lowest among miR-181a–d in glioma tissues and cell lines, and the low level of miR-181a was closely associated with the increased expression of Kaiso in glioma tissues. Moreover, transfection of miR-181a significantly inhibited the proliferation, invasion, and EMT of glioma cells, whereas knockdown of miR-181a had the opposite effect. Bioinformatics analysis predicted that Kaiso was a potential target gene of miR-181a, and the luciferase reporter assay demonstrated that miR-181a could directly target Kaiso. In addition, Kaiso silencing had similar effects as miR-181a overexpression in glioma cells, whereas overexpression of Kaiso in glioma cells partially reversed the inhibitory effects of the miR-181a mimic. Conclusionss miR-181a inhibited the proliferation, invasion, and EMT of glioma cells by directly targeting and downregulating Kaiso expression.
机译:背景/目的Kaiso(ZBTB33)的表达与许多癌症的进展和microRNA(miRNA)加工密切相关。 MiR-181a在多种癌症中起着至关重要的作用;然而,其在神经胶质瘤中的确切机制尚未得到很好的阐明。这项研究的目的是评估神经胶质瘤中Kaiso和miR-181a之间的相互作用。方法采用实时荧光定量PCR(qRT-PCR)检测胶质瘤组织和细胞株中Kaiso和miR-181a的水平。评估了细胞增殖,侵袭和上皮-间质转化(EMT),以分析神经胶质瘤细胞中miR-181a和Kaiso的生物学功能。 Kaiso的mRNA和蛋白质水平分别通过qRT-PCR和蛋白质印迹法测量。同时,进行荧光素酶测定以验证Kaiso作为神经胶质瘤细胞中的miR-181a靶标。结果我们发现,在胶质瘤组织和细胞系中,miR-181a的水平最低,而miR-181a的低水平与胶质瘤组织中Kaiso表达的增加密切相关。此外,转染miR-181a明显抑制神经胶质瘤细胞的增殖,侵袭和EMT,而敲低miR-181a具有相反的作用。生物信息学分析预测Kaiso是miR-181a的潜在靶基因,荧光素酶报告基因检测表明miR-181a可以直接靶向Kaiso。此外,Kaiso沉默与神经胶质瘤细胞中miR-181a的过表达具有相似的作用,而神经胶质瘤细胞中Kaiso的过表达可部分逆转miR-181a模拟物的抑制作用。结论miR-181a通过直接靶向和下调Kaiso表达来抑制神经胶质瘤细胞的增殖,侵袭和EMT。

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