The long noncoding RNA TUG1 acts as a competing endogenous RNA to regulate the Hedgehog pathway by targeting miR-132 in hepatocellular carcinoma
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Jingjing Li1, Qinghui Zhang2, Xiaoming Fan3, Wenhui Mo4, Weiqi Dai1, Jiao Feng1, Liwei Wu1, Tong Liu1, Sainan Li1, Shizan Xu5, Wenwen Wang1, Xiya Lu1, Qiang Yu5, Kan Chen1, Yujing Xia1, Jie Lu1, Yingqun Zhou1, Ling Xu6 and Chuanyong Guo1
1Department of Gastroenterology, Shanghai Tenth People’s Hospital, Tongji University School of Medicine, Shanghai 200072, China
2Department of Clinical Laboratory, Kunshan First People’s Hospital Affiliated to Jiangsu University, Kunshan 215300, China
3Department of Gastroenterology, Jinshan Hospital of Fudan University, Shanghai 201508, China
4Department of Gastroenterology, Minhang Hospital, Fudan University, Shanghai 201100, China
5Department of Gastroenterology, Shanghai Tenth Hospital School of Clinical Medicine of Nanjing Medical University, Shanghai 200072, China
6Department of Gastroenterology, Shanghai Tongren Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200336, China
Ling Xu, email: firstname.lastname@example.org
Chuanyong Guo, email: email@example.com
Keywords: Hedgehog, TUG1, miR-132, hepatocellular carcinoma
Received: April 25, 2017 Accepted: June 28, 2017 Published: July 26, 2017
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.
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