Department of Neurosurgery, Tangdu Hospital, Fourth Military Medical University, Xi'an, P.R. China.
Department of Neurosurgery, Xi'an Children's Hospital, Xi'an, P.R. China.
Oncol Res. 2018 Jan 19;26(1):103-110. doi: 10.3727/096504017X14934860122864. Epub 2017 May 5.
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.
神经胶质瘤是最常见和最致命的颅内恶性肿瘤。长链非编码 RNA（lncRNA）已被确定为神经胶质瘤发生的关键调节因子。然而，lncRNA 尿路上皮癌相关 1（UCA1）在神经胶质瘤发生中的作用尚不清楚。本研究旨在探讨 UCA1 在神经胶质瘤发生中的潜在作用。结果表明，UCA1 在神经胶质瘤组织中上调，并提示预后不良。通过 si-UCA1 下调 UCA1 显著抑制神经胶质瘤细胞系（U87 和 U251）的增殖、迁移和侵袭活性。生物信息学分析和荧光素酶报告基因实验验证了 UCA1 在 3'-UTR 与 miR-122 之间的互补结合。功能实验表明，UCA1 作为 miR-122 的“海绵”，通过下调 miR-122 来调节神经胶质瘤细胞的增殖、迁移和侵袭。总之，本研究表明 lncRNA UCA1 作为 miR-122 的内源性海绵，促进神经胶质瘤细胞的增殖、迁移和侵袭，为神经胶质瘤的发生提供了新的见解和治疗靶点。
