Knockdown of long non-coding RNA XIST increases blood-tumor barrier permeability and inhibits glioma angiogenesis by targeting miR-137

被引：104
|
作者：
Yu, H. [1 ,2 ]
Xue, Y. [3 ,4 ,5 ]
Wang, P. [3 ,4 ,5 ]
Liu, X. [1 ,2 ]
Ma, J. [3 ,4 ,5 ]
Zheng, J. [1 ,2 ]
Li, Z. [2 ,3 ,4 ,5 ]
Cai, H. [2 ]
Liu, Y. [1 ,2 ]
机构：
[1] China Med Univ, Shengjing Hosp, Dept Neurosurg, Shenyang 110004, Peoples R China
[2] Liaoning Res Ctr Translat Med Nervous Syst Dis, Shenyang, Peoples R China
[3] China Med Univ, Coll Basic Med, Dept Neurobiol, Shenyang, Peoples R China
[4] China Med Univ, Key Lab Cell Biol, Minist Publ Hlth China, Shenyang, Peoples R China
[5] China Med Univ, Key Lab Med Cell Biol, Minist Educ China, Shenyang, Peoples R China
来源：
ONCOGENESIS | 2017年 / 6卷
关键词：
CHEMOKINE RECEPTOR CXCR7; VEIN ENDOTHELIAL-CELLS; STEM-CELLS; SUPPRESSIVE FUNCTIONS; DOWN-REGULATION; IN-VITRO; PROMOTES; CANCER; GROWTH; EXPRESSION;
D O I：
10.1038/oncsis.2017.7
中图分类号：
R73 [肿瘤学];
学科分类号：
100214 ;
摘要：
Antiangiogenic therapy plays a significant role in combined glioma treatment. However, poor permeability of the blood-tumor barrier (BTB) limits the transport of chemotherapeutic agents, including antiangiogenic drugs, into tumor tissues. Long non-coding RNAs (lncRNAs) have been implicated in various diseases, especially malignant tumors. The present study found that lncRNA X-inactive-specific transcript (XIST) was upregulated in endothelial cells that were obtained in a BTB model in vitro. XIST knockdown increased BTB permeability and inhibited glioma angiogenesis. The analysis of the mechanism of action revealed that the reduction of XIST inhibited the expression of the transcription factor forkhead box C1 (FOXC1) and zonula occludens 2 (ZO-2) by upregulating miR-137. FOXC1 decreased BTB permeability by increasing the promoter activity and expression of ZO-1 and occludin, and promoted glioma angiogenesis by increasing the promoter activity and expression of chemokine (C-X-C motif) receptor 7b (CXCR7). Overall, the present study demonstrates that XIST plays a pivotal role in BTB permeability and glioma angiogenesis, and the inhibition of XIST may be a potential target for the clinical management of glioma.
引用
收藏
页码：e303 / e303
页数：11
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