Knockdown of Long Noncoding RNA LUCAT1 Inhibits Cell Viability and Invasion by Regulating miR-375 in Glioma

被引:49
作者
Gao, Yan-Sheng [1 ]
Liu, Xian-Zhi [2 ]
Zhang, Yong-Gang [1 ]
Liu, Xian-Jin [1 ]
Li, Ling-Zhen [3 ]
机构
[1] Zhumadian Cent Hosp, Dept Neurosurg, 747 Zhonghua Rd, Zhumadian 463000, Henan, Peoples R China
[2] Zhengzhou Univ, Affiliated Hosp 1, Dept Neurosurg, Zhengzhou, Henan, Peoples R China
[3] Zhumadian Cent Hosp, Dept Neurol, Zhumadian, Henan, Peoples R China
关键词
Long noncoding RNAs (lncRNAs); LUCAT1; miR-375; Glioma; Progression; POOR-PROGNOSIS; CANCER; PROLIFERATION; PROGRESSION; EPIDEMIOLOGY; EXPRESSION;
D O I
10.3727/096504017X15088061795756
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Recently, long noncoding RNAs (lncRNAs) have emerged as new gene regulators and prognostic markers in several cancers, including glioma. Here we focused on lncRNA LUCAT1 on the progression of glioma. qRT-PCR was used to determine the expression of LUCAT1 and miR-375 in glioma tissues and cells. MTT and Transwell invasion assays were performed to determine the function of LUCAT1 in glioma progression. The bioinformatics tool DIANA was used to predict the targets of LUCAT1. Pearson's correlation analysis was performed to explore the correlation between LUCAT1 and miR-375. In the present study, we showed that LUCAT1 was substantially upregulated in glioma tissues and cells. LUCAT1 inhibition significantly suppressed the proliferation and invasion of glioma cells. Subsequently, DIANA showed that miR-375 was predicted to contain the complementary binding sites to LUCAT1. Luciferase reporter assay showed that miR-375 directly targeted LUCAT1. In addition, we found that miR-375 was downregulated in glioma tissues and negatively correlated with LUCAT1 expression in glioma tissues. Furthermore, the results showed that miR-375 could rescue the function of LUCAT1 in glioma progression. The lncRNA LUCAT1 was critical for the proliferation and invasion of glioma cells by regulating miR-375. Our findings indicated that LUCAT1 might offer a potential novel therapeutic target for the treatment of glioma.
引用
收藏
页码:307 / 313
页数:7
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