The lncRNA TUG1 promotes epithelial ovarian cancer cell proliferation and invasion via the WNT/β-catenin pathway
Authors Liu S, Liu Y, Lu Q, Zhou X, Chen L, Liang W
Received 11 March 2018
Accepted for publication 30 May 2018
Published 12 October 2018 Volume 2018:11 Pages 6845—6851
Checked for plagiarism Yes
Review by Single-blind
Peer reviewer comments 3
Editor who approved publication: Dr Cho
This paper has been retracted
Shankun Liu,1 Ying Liu,1 Qiang Lu,2 Xiao Zhou,2 Li Chen,2 Weifeng Liang3
1Department of Gynecology, Tai’an City Center Hospital, Tai’an, Shandong, People’s Republic of China; 2Department of Obstetrics and Gynecology, The Affiliated Qingdao Hiser Hospital of Qingdao University (Qingdao Hospital of Traditional Chinese Medicine), Qingdao, Shandong, People’s Republic of China; 3Department of Obstetrics and Gynecology, Qilu Hospital, Shandong University, Qingdao, Shandong, People’s Republic of China
Purpose: Epithelial ovarian cancer (EOC) is among the most common malignant tumors of the endocrine system. Numerous studies have shown that genetic factors are important in the development of EOC, and there is evidence that long noncoding RNA molecules (lncRNAs) can regulate gene expression at the transcription, posttranscription, and epigenetic levels to influence cancer proliferation and invasion, cell differentiation, and apoptosis. However, the roles of lncRNAs in the pathogenesis of EOC remain unclear. Here, we investigated the role of the lncRNA, taurine upregulated gene 1 (TUG1), in EOC.
Patients and methods: TUG1 mRNA levels were evaluated in EOC and matched normal tissue samples and in EOC cell lines by quantitative real-time PCR. Lentiviral vectors expressing the lncRNA, TUG1, and siRNA targeting TUG1 were constructed and transfected into EOC cells. MTT and Transwell assays were used to determine the effects of TUG1 on cell proliferation, migration, and invasion. Western blotting was performed to determine the influence of TUG1 up- or downregulation on WNT/β-catenin signaling, which is involved in the occurrence and development of cancer.
Results: TUG1 expression was clearly elevated in EOC compared with control tissue and cells. Moreover, TUG1 expression was associated with lymphatic metastasis, T stage, and clinical stage in patients with EOC. Downregulation of TUG1 in EOC inhibited cell proliferation, migration, and invasion. In EOC cells, levels of the WNT/β-catenin pathway factors, β-catenin, cyclin D1, and c-Myc, were significantly up- and downregulated in response to TUG1 over- and underexpression, respectively.
Conclusion: Our data suggest that knockdown of TUG1 may represent a novel therapeutic approach for the management of EOC.
Keywords: epithelial ovarian cancer, long noncoding RNA, prognosis, molecular mechanisms
This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution - Non Commercial (unported, v3.0) License. By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms.Download Article [PDF] View Full Text [HTML][Machine readable]