// Jingjing Li 1 , Qinghui Zhang 2 , Xiaoming Fan 3 , Wenhui Mo 4 , Weiqi Dai 1 , Jiao Feng 1 , Liwei Wu 1 , Tong Liu 1 , Sainan Li 1 , Shizan Xu 5 , Wenwen Wang 1 , Xiya Lu 1 , Qiang Yu 5 , Kan Chen 1 , Yujing Xia 1 , Jie Lu 1 , Yingqun Zhou 1 , Ling Xu 6 and Chuanyong Guo 1 1 Department of Gastroenterology, Shanghai Tenth People’s Hospital, Tongji University School of Medicine, Shanghai 200072, China 2 Department of Clinical Laboratory, Kunshan First People’s Hospital Affiliated to Jiangsu University, Kunshan 215300, China 3 Department of Gastroenterology, Jinshan Hospital of Fudan University, Shanghai 201508, China 4 Department of Gastroenterology, Minhang Hospital, Fudan University, Shanghai 201100, China 5 Department of Gastroenterology, Shanghai Tenth Hospital School of Clinical Medicine of Nanjing Medical University, Shanghai 200072, China 6 Department of Gastroenterology, Shanghai Tongren Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200336, China Correspondence to: Ling Xu, email: xiaoling05@126.com Chuanyong Guo, email: guochuanyong@hotmail.com Keywords: Hedgehog, TUG1, miR-132, hepatocellular carcinoma Received: April 25, 2017 Accepted: June 28, 2017 Published: July 26, 2017 ABSTRACT 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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