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Long Noncoding RNA MEG3 Suppresses Glioma Cell Proliferation, Migration, and Invasion by Acting as a Competing Endogenous RNA of miR-19a

机译:长度非编码RNA Meg3抑制胶质瘤细胞增殖,迁移和侵袭通过作为MIR-19A的竞争内源性RNA

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摘要

Glioma, with varying malignancy grades and histological subtypes, is the most common primary brain tumor in adults. Long noncoding RNAs (lncRNAs) are non-protein-coding transcripts and have been proven to play an important role in tumorigenesis. Our study aims to elucidate the combined effect of lncRNA maternally expressed gene 3 (MEG3) and microRNA-19a (miR-19a) in human glioma U87 and U251 cell lines. Real-time PCR revealed that MEG3 was downregulated and miR-19a was upregulated in malignant glioma tissues and cell lines. Bioinformatics analyses (TargetScan, miRanda, and starBase V2.0) showed that phosphatase and tensin homolog (PTEN) is a target of miR-19a with complementary binding sites in the 3'-UTR. As expected, luciferase results verified the putative target site and also revealed the complementary binding between miR-19a and MEG3. miR-19a represses the expression of PTEN and promotes glioma cell proliferation, migration, and invasion. However, MEG3 could directly bind to miR-19a and effectively act as a competing endogenous RNA (ceRNA) for miR-19a to suppress tumorigenesis. Our study is the first to demonstrate that lncRNA MEG3 suppresses glioma cell proliferation, migration, and invasion by acting as a ceRNA of miR-19a, which provides a novel insight about the pathogenesis of glioma.
机译:具有不同恶性成绩和组织学亚型的胶质瘤是成年人中最常见的原发性脑肿瘤。长度非编码RNA(LNCRNA)是非蛋白质编码转录物,并且已被证明在肿瘤内酯中发挥重要作用。我们的研究旨在阐明LNCRNA母体表达基因3(MEG3)和MICRRNA-19A(MIR-19A)在人胶质瘤U87和U251细胞系中的综合作用。实时PCR揭示了MEG3下调,MIR-19A在恶性胶质瘤组织和细胞系中被上调。生物信息学分析(TargetScan,Miranda和Starbase v2.0)显示磷酸酶和硫素同源物(PTEN)是MIR-19a的靶标,其中3'-UTR中的互补结合位点。正如预期的那样,荧光素酶结果验证了推定的靶位点,并揭示了MIR-19A和MEG3之间的互补结合。 miR-19a压制PTEN的表达,促进胶质瘤细胞增殖,迁移和侵袭。然而,MEG3可以直接与miR-19a结合,并有效地作为miR-19a的竞争内源性RNA(Cerna),以抑制肿瘤发生。我们的研究是第一个证明LNCRNA MEG3通过作为MIR-19A的CERNA抑制胶质瘤细胞增殖,迁移和入侵,为胶质瘤的发病机制提供了一种新颖的洞察力。

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