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The long noncoding RNA TUG1 acts as a competing endogenous RNA to regulate the Hedgehog pathway by targeting miR-132 in hepatocellular carcinoma
被引:47
作者:
Li, Jingjing
[1
]
Zhang, Qinghui
[2
]
Fan, Xiaoming
[3
]
Mo, Wenhui
[4
]
Dai, Weiqi
[1
]
Feng, Jiao
Wu, Liwei
[1
]
Liu, Tong
[1
]
Li, Sainan
[1
]
Xu, Shizan
[5
]
Wang, Wenwen
[1
]
Lu, Xiya
[1
]
Yu, Qiang
[5
]
Chen, Kan
[1
]
Xia, Yujing
[1
]
Lu, Jie
[1
]
Zhou, Yingqun
[1
]
Xu, Ling
[6
]
Guo, Chuanyong
[1
]
机构:
[1] Tongji Univ, Dept Gastroenterol, Shanghai Peoples Hosp 10, Sch Med, Shanghai 200072, Peoples R China
[2] Jiangsu Univ, Dept Clin Lab, Kunshan Peoples Hosp 1, Kunshan 215300, Peoples R China
[3] Fudan Univ, Dept Gastroenterol, Jinshan Hosp, Shanghai 201508, Peoples R China
[4] Fudan Univ, Dept Gastroenterol, Minhang Hosp, Shanghai 201100, Peoples R China
[5] Nanjing Med Univ, Dept Gastroenterol, Shanghai Hosp 10, Sch Clin Med, Shanghai 200072, Peoples R China
[6] Shanghai Jiao Tong Univ, Dept Gastroenterol, Shanghai Tongren Hosp, Sch Med, Shanghai 200336, Peoples R China
来源:
基金:
中国国家自然科学基金;
关键词:
Hedgehog;
TUG1;
miR-132;
hepatocellular carcinoma;
SIGNALING PATHWAY;
LIVER FIBROSIS;
CANCER;
EXPRESSION;
CELLS;
PROLIFERATION;
HEPATOCARCINOGENESIS;
MICRORNA-132;
SUPPRESSES;
MIGRATION;
D O I:
10.18632/oncotarget.19582
中图分类号:
R73 [肿瘤学];
学科分类号:
100214 ;
摘要:
Emerging evidence shows that the Hedgehog pathway and the long noncoding RNA TUG1 play pivotal roles in cell proliferation, migration, and invasion in tumors. However, the mechanism underlying the effect of TUG1 and the Hedgehog pathway in hepatoma remains undefined. In the present study, we showed that the expression of TUG1 was negatively correlated with that of microRNA (miR)-132, and depletion of TUG1 inhibited the activation of the Hedgehog pathway in vitro and in vivo. We showed that TUG1 functions as a competing endogenous (ceRNA) by competing with miR-132 for binding to the sonic hedgehog protein in HCC, thereby suppressing the activation of Hedgehog signaling and its tumorigenic effect. These data indicate that targeting the TUG1-miR132-Hedgehog network could be a new strategy for the treatment of HCC.
引用
收藏
页码:65932 / 65945
页数:14
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