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of Long Noncoding RNA LINC00152 Suppresses Cellular Proliferation and Invasion in Glioma Cells by Regulating miR-4775 (Withdrawn Publication)

被引:17
|
作者
Zhu, Zhankun [1 ]
Dai, Jinhua [1 ]
Liao, Yufeng [1 ]
Ma, Jianbo [1 ]
Zhou, Wei [2 ]
机构
[1] Ningbo 2 Hosp, Dept Clin Lab, Ningbo, Zhejiang, Peoples R China
[2] Ningbo 2 Hosp, Dept Neurosurg, 41 Xibei St, Ningbo 315010, Zhejiang, Peoples R China
关键词
Long intergenic noncoding RNA 152 (LINC00152); MicroRNA 4775 (miR-4775); Glioma; Proliferation; Metastasis; Apoptosis; BIOLOGICAL BEHAVIOR; GLIOBLASTOMA CELLS; CDK6; EXPRESSION; PROGRESSION; METASTASIS; CARCINOMA; GROWTH;
D O I
10.3727/096504017X15016337254597
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
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.
引用
收藏
页码:857 / 867
页数:11
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