1. Long Noncoding RNA UCA1 Targets miR-122 to Promote Proliferation, Migration, and Invasion of Glioma Cells
- Author
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Yang Sun, Jun-Gong Jin, Wei-Yang Mi, null Hao-Wu, Shi-Rong Zhang, Qiang Meng, and Shi-Tao Zhang
- Subjects
0301 basic medicine ,Cancer Research ,Urothelial carcinoma-associated 1 (UCA1) ,Biology ,medicine.disease_cause ,Article ,03 medical and health sciences ,0302 clinical medicine ,Downregulation and upregulation ,Invasion ,Cell Movement ,Cell Line, Tumor ,Glioma ,MiR-122 ,medicine ,Humans ,Neoplasm Invasiveness ,neoplasms ,Migration ,Cell Proliferation ,Regulation of gene expression ,Gene knockdown ,Brain Neoplasms ,Long noncoding RNAs (lncRNAs) ,General Medicine ,medicine.disease ,Molecular biology ,Long non-coding RNA ,nervous system diseases ,miR-122 ,Gene Expression Regulation, Neoplastic ,MicroRNAs ,Cell Transformation, Neoplastic ,030104 developmental biology ,Oncology ,Cell culture ,030220 oncology & carcinogenesis ,Cancer research ,RNA, Long Noncoding ,Erratum ,Carcinogenesis - Abstract
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. An erratum for this article has been published in Oncology Research, Volume 28, Number 6, pp.683-684 (https://www.ingentaconnect.com/contentone/cog/or/2021/00000028/00000006/art00011). Note that an updated article PDF will be delivered from this page further to the issuing of the erratum.
- Published
- 2018