Targeting long non-coding RNA-TUG1 inhibits tumor growth and angiogenesis in hepatoblastoma

被引:103
|
作者
Dong, R. [1 ,2 ,3 ]
Liu, G-B [1 ]
Liu, B-H [1 ]
Chen, G. [1 ]
Li, K. [1 ,2 ,3 ]
Zheng, S. [1 ,2 ,3 ]
Dong, K-R [1 ,2 ,3 ]
机构
[1] Fudan Univ, Childrens Hosp, Dept Pediat Surg, 399 Wan Yuan Rd, Shanghai 201102, Peoples R China
[2] Shanghai Key Lab Birth Defect, Shanghai, Peoples R China
[3] Minist Hlth, Key Lab Neonatal Dis, Shanghai, Peoples R China
来源
CELL DEATH & DISEASE | 2016年 / 7卷
基金
中国国家自然科学基金;
关键词
DOWN-REGULATION; RNA TUG1; CELL-PROLIFERATION; CANCER; EXPRESSION; PATHWAYS; GENETICS; DISEASE; MIR-34; VEGF;
D O I
10.1038/cddis.2016.143
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Hepatoblastoma is the most common liver tumor of early childhood, which is usually characterized by unusual hypervascularity. Recently, long non-coding RNAs (lncRNA) have emerged as gene regulators and prognostic markers in several cancers, including hepatoblastoma. We previously reveal that lnRNA-TUG1 is upregulated in hepatoblastoma specimens by microarray analysis. In this study, we aim to elucidate the biological and clinical significance of TUG1 upregulation in hepatoblastoma. We show that TUG1 is significantly upregulated in human hepatoblastoma specimens and metastatic hepatoblastoma cell lines. TUG1 knockdown inhibits tumor growth and angiogenesis in vivo, and decreases hepatoblastoma cell viability, proliferation, migration, and invasion in vitro. TUG1, miR-34a-5p, and VEGFA constitutes to a regulatory network, and participates in regulating hepatoblastoma cell function, tumor progression, and tumor angiogenesis. Overall, our findings indicate that TUG1 upregulation contributes to unusual hypervascularity of hepatoblastoma. TUG1 is a promising therapeutic target for aggressive, recurrent, or metastatic hepatoblastoma.
引用
收藏
页码:e2278 / e2278
页数:13
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