Long non-coding RNA TUG1 regulates ovarian cancer proliferation and metastasis via affecting epithelial-mesenchymal transition

被引:73
作者
Kuang, Defeng [1 ]
Zhang, Xiaoping [3 ]
Hua, Shaofang [1 ]
Dong, Wei [1 ]
Li, Zhiguo [2 ]
机构
[1] Tianjin Med Univ, Hosp 2, Dept Obstet, Tianjin, Peoples R China
[2] Tianjin Med Univ, Hosp 2, Dept Clin Lab, 23 Pingjiang St, Tianjin 300211, Peoples R China
[3] Fourth Peoples Hosp, Dept Clin Lab, Xian, Shaanxi Provinc, Peoples R China
关键词
Ovarian cancer; TUG1; Cell proliferation; Cell invasion; Cell apoptosis; Epithelial-mesenchymal transition; POOR-PROGNOSIS; CELL-GROWTH; APOPTOSIS; EXPRESSION; RESISTANCE; CARCINOMA; SPONGE; MATTER; EMT;
D O I
10.1016/j.yexmp.2016.09.008
中图分类号
R36 [病理学];
学科分类号
100104 ;
摘要
Ovarian cancer is the fifth leading cause of cancer-related death in women worldwide, and recent studies have highlighted the role of long non-coding RNAs (lncRNAs) in cancer development. However, the role of lncRNAs in ovarian cancer is largely unclear. In this study, we focused on the taurine up-regulated gene 1 (TUG1) and examined its molecular mechanism in ovarian cancer. Here, we reported that TUGI was up-regulated in ovarian cancer tissues and ovarian cancer cells, and TUGI expression was positively correlated with tumor grade and FIGO stage. In vitro functional assays (CCK-8 assay, colony formation assay, and cell invasion assay) revealed that knock-down of TUG1 by small RNA inference significantly inhibited cell proliferation, colony formation and cell invasion in ovarian cancer cells. Further experiment showed that knock-down of TUG1 induced cell apoptosis and altered the protein expression levels of apoptosis-related mediators in ovarian cancer cells. More importantly, knock-down of TUG1 also reversed epithelial-mesenchymal transition in ovarian cancer. In summary, our results suggest that knock-down of TUGI may represent a novel therapeutic strategy for the treatment of ovarian cancer. (C) 2016 Elsevier Inc. All rights reserved.
引用
收藏
页码:267 / 273
页数:7
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