Long non-coding RNA CCAT2 promotes gastric cancer proliferation and invasion by regulating the E-cadherin and LATS2.

Dysregulation of long non-coding RNAs (lncRNAs) play important roles in tumor development and progression. The long non-coding RNA CCAT2 has been identified to be up-regulated in gastric cancer (GC). However, the detailed molecular mechanism of CCAT2 involved in GC progression is still unknown. The aim of this study was to explore the expression and role of CCAT2 in GC progression. In the study, the expression levels of CCAT2 were significantly up-regulated in 108 cases GC tissues compared with adjacent non-tumor tissues by qRT-PCR analysis. Higher CCAT2 expression was correlated with tumor size, lymph node metastasis and Tumor Node Metastasis (TNM) stage in GC patients. Multivariate analysis showed that lymph node metastasis, TNM stage and the expression of CCAT2 were independent prognostic indicator for disease-free survival (DFS) and the over survival time (OS) for GC patients. Further function analysis demonstrated that knockdown of CCAT2 inhibited the cell migration and invasion, whereas, the overexpression of CCAT2 showed the opposite results in GC cells. Our results also demonstrated that CCAT2 promoted the GC cells epithelial-mesenchymal transition (EMT) by downregulated the E-cadherin expression and upregulated the ZEB2, Vimentin and N-cadherin expression. Moreover, RNA immunoprecipitation (RIP) and Chromatin immunoprecipitation (ChIP) revealed that CCAT2 interacted with EZH2 and regulated the E-cadherin and LATS2 expression. Thus, our results demonstrated that CCAT2 functioned as an oncogene in GC and was involved in gastric cancer progression. Targeting CCAT2 might be a potential therapeutic target for GC.