The prognostic potential and carcinogenesis of long non-coding RNA TUG1 in human cholangiocarcinoma
PDF | HTML | How to cite
Metrics: PDF 1137 views | HTML 2127 views | ?
Yi Xu1,2, Kaiming Leng1, Zhenglong Li1,2, Fumin Zhang1,2, Xiangyu Zhong1, Pengcheng Kang1, Xingming Jiang1 and Yunfu Cui1
1Department of Hepatopancreatobiliary Surgery, Second Affiliated Hospital of Harbin Medical University, Harbin, China
2Department of The Key Laboratory of Myocardial Ischemia, Harbin Medical University, Ministry of Education, Harbin, China
Yunfu Cui, email: [email protected]
Xingming Jiang, email: [email protected]
Keywords: cholangiocarcinoma, lncRNA, TUG1, prognosis, EMT
Received: February 02, 2017 Accepted: June 30, 2017 Published: July 22, 2017
Cholangiocarcinoma (CCA) is a fatal disease with increasing worldwide incidence and is characterized by poor prognosis due to its poor response to conventional chemotherapy or radiotherapy. Long non-coding RNAs (lncRNAs) play key roles in multiple human cancers, including CCA. Cancer progression related lncRNA taurine-up-regulated gene 1 (TUG1) was reported to be involved in human carcinomas. However, the impact of TUG1 in CCA is unclear. The aim of this study was to explore the expression pattern of TUG1 and evaluate its clinical significance as well as prognostic potential in CCA. In addition, the functional roles of TUG1 including cell proliferation, apoptosis, migration, invasion and epithelial-mesenchymal transition (EMT), were evaluated after TUG1 silencing. Our data demonstrated up-regulation of TUG1 in both CCA tissues and cell lines. Moreover, overexpression of TUG1 is linked to tumor size (p=0.005), TNM stage (p=0.013), postoperative recurrence (p=0.036) and overall survival (p=0.010) of CCA patients. Furthermore, down-regulation of TUG1 following RNA silencing reduced cell growth and increased apoptosis in CCA cells. Additionally, TUG1 suppression inhibited metastasis potential in vitro by reversing EMT. Overall, our results suggest that TUG1 may be a rational CCA-related prognostic factor and therapeutic target.
All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 3.0 License.