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Long Noncoding RNA UCA1 Targets miR-122 to Promote Proliferation, Migration, and Invasion of Glioma Cells

机译:长的非编码RNA UCA1靶向miR-122,以促进胶质瘤细胞的增殖,迁移和侵袭

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摘要

Glioma is the most common and lethal malignant intracranial tumor. Long noncoding RNAs (lncRNAs) have been identified as pivotal regulators in the tumorigenesis of glioma. However, the role of lncRNA urothelial carcinoma-associated 1 (UCA1) in glioma genesis is still unknown. The purpose of this study was to investigate the underlying function of UCA1 on glioma genesis. The results demonstrated that UCA1 was upregulated in glioma tissue and indicated a poor prognosis. UCA1 knockdown induced by si-UCA1 significantly suppressed the proliferative, migrative, and invasive activities of glioma cell lines (U87 and U251). Bioinformatics analysis and luciferase reporter assay verified the complementary binding within UCA1 and miR-122 at the 3'-UTR. Functional experiments revealed that UCA1 acted as an miR-122 "sponge" to modulate glioma cell proliferation, migration, and invasion via downregulation of miR-122. Overall, the present study demonstrated that lncRNA UCA1 acts as an endogenous sponge of miR-122 to promote glioma cell proliferation, migration, and invasion, which provides a novel insight and therapeutic target in the tumorigenesis of glioma.
机译:胶质瘤是最常见和最致命的恶性颅内肿瘤。长度非编码RNA(LNCRNA)已被鉴定为胶质瘤的肿瘤瘤中的枢转调节剂。然而,LNCRNA尿路上皮癌相关1(UCA1)在胶质瘤成因中的作用仍然未知。本研究的目的是研究UCA1对胶质瘤成因的潜在功能。结果表明,UCA1在胶质瘤组织中上调并表明预后差。 Si-UCA1诱导的UCA1敲低显着抑制了胶质瘤细胞系(U87和U251)的增殖性,迁移和侵入性活性。生物信息学分析和荧光素酶报告器测定验证了在3'-UTR的UCA1和miR-122内的互补结合。功能实验表明,UCA1通过MIR-122的下调来调节胶质瘤细胞增殖,迁移和侵袭的miR-122“海绵”。总体而言,本研究表明,LNCRNA UCA1充当MIR-122的内源海绵,以促进胶质瘤细胞增殖,迁移和侵袭,这在胶质瘤的肿瘤瘤中提供了一种新的见解和治疗靶标。

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