首页> 外文期刊>OncoTargets and therapy >Long Noncoding RNA SNHG16 Sponges miR-182-5p And miR-128-3p To Promote Retinoblastoma Cell Migration And Invasion By Targeting LASP1
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Long Noncoding RNA SNHG16 Sponges miR-182-5p And miR-128-3p To Promote Retinoblastoma Cell Migration And Invasion By Targeting LASP1

机译:长非编码RNA SNHG16海绵miR-182-5p和miR-128-3p通过靶向LASP1促进视网膜母细胞瘤细胞迁移和侵袭

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Background: Long noncoding RNAs (lncRNAs) are dysregulated and play an important role in the tumorigenesis and progression of cancers. However, the potential roles of SNHG16 in retinoblastoma progression still remain largely unclear. Materials and methods: The expression levels of SNHG16, miR-182-5p, miR-128-3p and LASP1 in retinoblastoma tissues and cell lines were detected using qRT-PCR. The migratory and invasive abilities of retinoblastoma cells were assessed using Transwell assay. The regulatory relationships among SNHG16, miR-182-5p, miR-128-3p and LASP1 were analyzed through bioinformatics prediction and validated by luciferase reporter assay and Western blot. Results: Here, we demonstrated that SNHG16 was frequently up-regulated in retinoblastoma tissue samples and cell lines. Clinicopathological features showed that high levels of SNHG16 were significantly associated with retinoblastoma metastasis and predicted poor overall survival. Functional studies demonstrated that knockdown of SNHG16 suppressed retinoblastoma cell migration and invasion. Mechanistic investigation revealed that SNHG16 exerted its oncogenic activity through increasing LASP1 expression and sponging miR-182-5p and miR-128-3p. Conclusion: Taken together, our findings suggest SNHG16 as a novel biomarker and therapeutic target against retinoblastoma.
机译:背景:长非编码RNA(lncRNA)失调,在癌症的发生和发展中起重要作用。但是,尚不清楚SNHG16在视网膜母细胞瘤进展中的潜在作用。材料和方法:用qRT-PCR检测SNHG16,miR-182-5p,miR-128-3p和LASP1在视网膜母细胞瘤组织和细胞系中的表达水平。使用Transwell测定法评估视网膜母细胞瘤细胞的迁移和侵袭能力。通过生物信息学预测分析了SNHG16,miR-182-5p,miR-128-3p和LASP1之间的调控关系,并通过荧光素酶报告基因分析和Western印迹法进行了验证。结果:在这里,我们证明了SNHG16在视网膜母细胞瘤组织样品和细胞系中经常被上调。临床病理特征表明,高水平的SNHG16与视网膜母细胞瘤转移显着相关,并预测整体存活率较差。功能研究表明,敲除SNHG16可抑制成视网膜细胞瘤细胞迁移和侵袭。机理研究表明,SNHG16通过增加LASP1表达和使miR-182-5p和miR-128-3p变海绵发挥其致癌活性。结论:综上所述,我们的发现表明SNHG16是一种新型的生物标志物,是抗视网膜母细胞瘤的治疗靶标。

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