Long non-coding RNA CCAT2 promotes cholangiocarcinoma cells migration and invasion by induction of epithelial-to-mesenchymal transition.

Cholangiocarcinoma (CCA) is one of the most aggressive malignancies in humans. Emerging evidence has indicated that abnormally expressed long non-coding RNAs (lncRNAs) could conduce to tumorigenesis and progression. Specifically, colon cancer-associated transcript 2 (CCAT2) has been reported to be overexpressed in several carcinomas. However, its clinical significance and functional roles in CCA is still unknown. qRT-PCR experiments were conducted to assess the CCAT2 expression in CCA tissue samples and cell lines. In addition, the link between CCAT2 expression and clinicopathological characteristics was analyzed. The potential effects of CCAT2 in CCA cells was evaluated in vitro including cell proliferation, colony-forming ability, apoptosis, migration, invasion and epithelial-to-mesenchymal transition (EMT). As a result, CCAT2 was aberrantly overexpressed in CCA tissue samples and cells, and this upregulation was correlated with tumor size, lymph node invasion, TNM stage and postoperative recurrence in CCA patients. Overexpression of CCAT2 could serve as an independent prognostic indicator for CCA. Additionally, overexpression of CCAT2 was a dismal prognostic indicator for patients with CCA. Furthermore, CCAT2 silencing caused tumor suppressive effects via reducing cell proliferation, migration and invasion, inducing cell apoptosis and reversing the EMT process in HuCCT1 and CCLP1 cells. Collectively, our data illustrated that lncRNA CCAT2 played an oncogenic role in CCA and may offer a potential therapeutic target for treating this fatal disease.