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Knockdown of Long Noncoding RNA LINC00152 Suppresses Cellular Proliferation and Invasion in Glioma Cells by Regulating miR-4775

机译:长度非划分RNA LINC00152的敲低通过调节miR-4775来抑制细胞增殖和胶质瘤细胞中的侵袭

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Long noncoding RNAs (IncRNAs) play an important role in various biological properties of glioma cells. Herein we aimed to elucidate the function and the possible molecular mechanisms of long intergenic noncoding RNA 152 (LINC00152) in glioma cells. Relative expressions of LINC00152, miR-4775, and CDK6 in U-118 MG cells were regulated by transfections. Thereafter, cell viability, migration. invasion, and apoptosis were analyzed by CCK-8, Transwell, and flow cytometry assays. Dual-Luciferase Reporter Assay was conducted to validate the target genes of LINC00152 and miR-4775. Expression of components of the signal pathways were detected by Western blot. The results showed that LINC00152 knockdown significantly suppressed cell viability, migration, and invasion and induced apoptosis in vitro. Additionally. LINC00152 functioned as a molecular sponge for miR-4775, and inhibition of miR-4775 reversed the tumor-suppressive effects of LINC00152 knockdown on glioma cells. Furthermore, CDK6 was confirmed to be a target of miR-4775, and overexpression of CDK6 reduced apoptosis and abolished the inhibitory effects of miR-4775 overexpression on cell viability, migration. and invasion. Overexpression of CDK6 activated the PI3K/AKT/MAPK and Notch signal pathways. Overall, these findings demonstrate that LINC00152 plays an oncogenic role in glioma cells by regulation of miR-4775, which may therefore be a potential therapeutic target for glioma.
机译:长度非编码RNA(Incrnas)在胶质瘤细胞的各种生物学性质中起重要作用。在此我们旨在阐明胶质瘤细胞中长性非基质非编码RNA 152(LINC00152)的功能和可能的分子机制。通过转染对U-118mg细胞中的LINC00152,miR-4775和CDK6的相对表达进行调节。此后,细胞活力,迁移。通过CCK-8,Transwell和流式细胞术测定分析侵袭和细胞凋亡。进行双荧光素酶报告器测定以验证LINC00152和MIR-4775的靶基因。通过Western印迹检测信号途径的组分的表达。结果表明,在体外,LINC00152显着抑制细胞活力,迁移和侵袭和诱导细胞凋亡。此外。 LINC00152用作MIR-4775的分子海绵,并抑制miR-4775逆转了LINC00152敲低对胶质瘤细胞的肿瘤抑制作用。此外,CDK6被证实是miR-4775的靶标,并且CDK6的过表达降低了凋亡,并废除了miR-4775过表达对细胞活力,迁移的抑制作用。和入侵。 CDK6的过度表达激活了PI3K / AKT / MAPK和NOTCH信号途径。总体而言,这些研究结果表明,LINC00152通过调节MiR-4775在胶质瘤细胞中起着致癌作用,因此可能是胶质瘤的潜在治疗靶标。

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