Knockdown of long non-coding RNA HOTAIR inhibits malignant biological behaviors of human glioma cells via modulation of miR-326

被引:175
作者
Ke, Jing [1 ,2 ]
Yao, Yi-long [3 ]
Zheng, Jian [3 ]
Wang, Ping [1 ,2 ]
Liu, Yun-hui [3 ]
Ma, Jun [1 ,2 ]
Li, Zhen [3 ]
Liu, Xiao-bai [3 ]
Li, Zhi-qing [1 ,2 ]
Wang, Zhen-hua [4 ]
Xue, Yi-xue [1 ,2 ]
机构
[1] China Med Univ, Coll Basic Med, Dept Neurobiol, Shenyang 110122, Peoples R China
[2] China Med Univ, Inst Pathol & Pathophysiol, Shenyang 110122, Peoples R China
[3] China Med Univ, Shengjing Hosp, Dept Neurosurg, Shenyang 110004, Peoples R China
[4] China Med Univ, Coll Basic Med, Dept Physiol, Shenyang 110122, Peoples R China
关键词
lncRNA; HOTAIR; miR-326; glioma; FGF1; FIBROBLAST GROWTH-FACTORS; POOR-PROGNOSIS; CANCER; EXPRESSION; PROTEIN; IDENTIFICATION; METASTASIS; ACTIVATION; INVASION; SURVIVAL;
D O I
10.18632/oncotarget.4290
中图分类号
R73 [肿瘤学];
学科分类号
100214 [肿瘤学];
摘要
Glioma is the most common and aggressive primary adult brain tumor. Long non-coding RNAs (lncRNAs) have important roles in a variety of biological properties of cancers. Here, we elucidated the function and the possible molecular mechanisms of lncRNA HOTAIR in human glioma U87 and U251 cell lines. Quantitative RT-PCR demonstrated that HOTAIR expression was up-regulated in glioma tissues and cell lines. Knockdown of HOTAIR exerted tumor-suppressive function in glioma cells. Further, HOTAIR was confirmed to be the target of miR-326 and miR-326 mediated the tumor-suppressive effects of HOTAIR knockdown on glioma cell lines. Moreover, over-expressed miR-326 reduced the FGF1 expression which played an oncogenic role in glioma by activating PI3K/AKT and MEK 1/2 pathways. In addition, the in vivo studies also supported the above findings. Taken together, knockdown of HOTAIR up-regulated miR-326 expression, and further inducing the decreased expression of FGF1, these results provided a comprehensive analysis of HOTAIR-miR-326-FGF1 axis in human glioma and provided a new potential therapeutic strategy for glioma treatment.
引用
收藏
页码:21934 / 21949
页数:16
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