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Knockdown of Long Noncoding RNA LUCAT1 Inhibits Cell Viability and Invasion by Regulating miR-375 in Glioma

机译:长度非数性RNA Lucat1的敲低通过调节胶质瘤中的miR-375来抑制细胞活力和侵袭

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摘要

Recently, long noncoding RNAs (lncRNAs) have emerged as new gene regulators and prognostic markers in several cancers, including glioma. Here we focused on lncRNA LUCAT1 on the progression of glioma. qRT-PCR was used to determine the expression of LUCAT1 and miR-375 in glioma tissues and cells. MTT and Transwell invasion assays were performed to determine the function of LUCAT1 in glioma progression. The bioinformatics tool DIANA was used to predict the targets of LUCAT1. Pearson's correlation analysis was performed to explore the correlation between LUCAT1 and miR-375. In the present study, we showed that LUCAT1 was substantially upregulated in glioma tissues and cells. LUCAT1 inhibition significantly suppressed the proliferation and invasion of glioma cells. Subsequently, DIANA showed that miR-375 was predicted to contain the complementary binding sites to LUCAT1. Luciferase reporter assay showed that miR-375 directly targeted LUCAT1. In addition, we found that miR-375 was downregulated in glioma tissues and negatively correlated with LUCAT1 expression in glioma tissues. Furthermore, the results showed that miR-375 could rescue the function of LUCAT1 in glioma progression. The lncRNA LUCAT1 was critical for the proliferation and invasion of glioma cells by regulating miR-375. Our findings indicated that LUCAT1 might offer a potential novel therapeutic target for the treatment of glioma.
机译:最近,长时间的NOCODING RNA(LNCRNA)被出现为新的基因调节因子和几种癌症中的预后标志物,包括胶质瘤。在这里,我们专注于LNCRNA Lucat1对胶质瘤的进展。 QRT-PCR用于测定胶质瘤组织和细胞中Lucat1和miR-375的表达。进行MTT和Transwell侵袭测定以确定Lucat1在胶质瘤进展中的功能。生物信息学工具Diana用于预测Lucat1的目标。进行Pearson的相关性分析,以探讨Lucat1和MiR-375之间的相关性。在本研究中,我们表明Lucat1在胶质瘤组织和细胞中基本上升高。 Lucat1抑制显着抑制了胶质瘤细胞的增殖和侵袭。随后,Diana显示MiR-375预计将含有互补的结合位点含有Lucat1。荧光素酶报告器测定显示MiR-375直接靶向液体1。此外,我们发现MiR-375在胶质瘤组织中下调,并与胶质瘤组织中的泻涂层表达呈负相关。此外,结果表明,MIR-375可以拯救泻淋巴瘤进展中的抑制功能。 LNCRNA Lucat1对于通过调节miR-375来激发胶质瘤细胞的增殖和侵袭至关重要。我们的研究结果表明,Lucat1可能为治疗胶质瘤提供潜在的新疗法靶标。

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