Abstract

Emerging evidence has classified the aberrant expression of long non-coding RNAs (lncRNAs) as a basic signature of various malignancies including gastric cancer (GC). LINC01225 has been shown to act as a hepatocellular carcinoma-related gene, with its expression pattern and biological function not clarified in GC. Here, we verified that LINC01225 was up-regulated in tumour tissues and plasma of GC. Analysis with clinicopathological information suggested that up-regulation of LINC01225 was associated with advanced disease and poorer overall survival. Receiver operating characteristic (ROC) analysis showed that plasma LINC01225 had a moderate accuracy for diagnosis of GC. In addition, knockdown of LINC01225 led to retardation of cell proliferation, invasion and migration, and overexpression of LINC01225 showed the opposite effects. Mechanistic investigations showed that LINC01225 silencing inhibited epithelial-mesenchymal transition (EMT) process and attenuated Wnt/β-catenin signalling of GC. Furthermore, ectopic expression of Wnt1 or suppression of GSK-3β abolished the si-LINC01225-mediated suppression against EMT, thereby promoting cell proliferation, invasion and migration of GC. In conclusion, LINC01225 promotes the progression of GC through Wnt/β-catenin signalling pathway, and it may serve as a potential target or strategy for diagnosis or treatment of GC.