lncRNA VIM-AS1 promotes cell proliferation, metastasis and epithelial-mesenchymal transition by activating the Wnt/β-catenin pathway in gastric cancer

The present study aimed to explore the biological functions and molecular mechanisms of the long non-coding RNA VIM antisense RNA 1 (VIM-AS1) in gastric cancer (GC). The expression of VIM-AS1 was analyzed in tissues from patients with GC and GC cell lines by reverse transcription-quantitative (RT-q)PCR. The relationship between VIM-AS1 expression and overall survival time of patients with GC was also assessed. To determine the biological functions of VIM-AS1, Cell Counting Kit-8 assay, colony formation assay, flow cytometry, wound healing assay and Transwell assay were employed. The targeting relationship among VIM-AS1, microRNA (miR)-8052 and frizzled 1 (FZD1) was verified by the dual luciferase reporter gene assay. The underlying molecular mechanism of VIM-AS1 on GC was determined by RT-qPCR and western blotting. In addition, tumor formation was detected in nude mice. The results of the present study demonstrated that VIM-AS1 was highly expressed in GC tissues and cells. In addition, VIM-AS1 expression was demonstrated to be closely related to the prognosis of patients with GC. Notably, silencing VIM-AS1 inhibited the proliferation, migration and invasion, and enhanced apoptosis of AGS and HGC-27 cells. Silencing VIM-AS1 significantly increased the protein expression levels of cleaved caspase-3, Bax and E-cadherin, but decreased the protein expression levels of Bcl-2, N-cadherin, vimentin, matrix metalloproteinase (MMP)-2, MMP-9, beta-catenin, cyclin D1, C-myc and FZD1. Additionally, silencing VIM-AS1 inhibited tumor growth in nude mice. Cumulatively, the present study demonstrated that VIM-AS1 may promote cell proliferation, migration, invasion and epithelial-mesenchymal transition by regulating FDZ1 and activating the Wnt/beta-catenin pathway in GC.