The lncRNA TUG1 promotes epithelial ovarian cancer cell proliferation and invasion via the WNT/β-catenin pathway

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 FOC, 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, Marine 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/beta-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/beta-catenin pathway factors, beta-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.