Silencing CCAT2 inhibited proliferation and invasion of epithelial ovarian carcinoma cells by regulating Wnt signaling pathway

Long non-coding RNA CCAT2 (colon cancer-associated transcript 2) is dysregulated in varieties of human tumors. However, the role of CCAT2 in epithelial ovarian carcinoma (EOC) is not yet known clearly. The aim of this study is to investigate the effects of CCAT2 on proliferation and invasion of EOC cells and the potential mechanisms by which CCAT2 functions. In the present paper, we found that knockdown of CCAT2 impaired cell proliferation and invasion in vitro. Furthermore, we also studied the role of CCAT2 in the modulation of Wnt/beta-catenin signaling pathway. Our results showed that knockdown of CCAT2 inhibited the expression of beta-catenin and the activity of TCF/LEF (T-cell factor/lymphoid enhancer factor) acting as a key transcription factor of Wnt/beta-catenin signaling pathway. In addition, we found that silencing CCAT2 down-regulated the expression of c-MYC and MMP-7. But, that was reversed by the treatment with LiCl (lithium chloride) which could activate canonical Wnt/beta-catenin signaling pathway. Taken together, these results indicate that CCAT2 may promote ovarian cancer progression, at least partly, through Wnt/beta-catenin signaling pathway. Thus, CCAT2 might represent a novel therapeutic target for ovarian cancer.