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, β‑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/β‑catenin pathway in GC.