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

Onco Targets Ther

Department of Obstetrics and Gynecology, Qilu Hospital, Shandong University, Qingdao, Shandong, People's Republic of China,

Published: October 2018

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 (), in EOC.

Patients And Methods: 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, , and siRNA targeting were constructed and transfected into EOC cells. MTT and Transwell assays were used to determine the effects of on cell proliferation, migration, and invasion. Western blotting was performed to determine the influence of up- or downregulation on WNT/β-catenin signaling, which is involved in the occurrence and development of cancer.

Results: expression was clearly elevated in EOC compared with control tissue and cells. Moreover, expression was associated with lymphatic metastasis, T stage, and clinical stage in patients with EOC. Downregulation of 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 over- and underexpression, respectively.

Conclusion: Our data suggest that knockdown of may represent a novel therapeutic approach for the management of EOC.

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6190633PMC
http://dx.doi.org/10.2147/OTT.S167900DOI Listing

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