RBMS3 inhibits invasion and epithelial-mesenchymal transition of gastric cancer cells via regulating Wnt/β-catenin signal pathway

Objective: To investigate the effect of RNA-binding motif, single-stranded-interacting protein 3 (RBMS3) on the invasion of gastric cancer cells, and to explore its possible action mechanism. Methods: The expression levels of RBMS3 mRNA and protein in human normal gastric mucosa epithelial cells (GES-1) and gastric cancer cells (MKN-28, MKN-45, NCI-N87 and SGC-7901) were detected by real-time fluorescent quantitative PCR (RFQ-PCR) and Western blotting, respectively. The RBMS3 overexpression vectors [RBMS3-pcDNA3.1(+)] were transfected into gastric cancer MKN-45 and SGC-7901 cells by using LipofectAMINE 2000, while the corresponding empty vector-transfection group and untransfection group were arranged as the negative control and blank control, respectively. The efficiency of RBMS3 overexpression was verified by RFQ-PCR and Western blotting. The cell invasion ability was detected by Transwell assay. The expression levels of epithelial-mesenchymal transition-related proteins and Wnt signal pathway protein β-catenin were detected by RFQ-PCR and Western blotting. After RBMS3 overexpressed MKN-45 and SGC-7901 cells were treated with Wnt pathway agonist lithium chloride (LiCl), the change of cell invasion ability was retested by Transwell assay.  Results: The mRNA and protein levels of RBMS3 in 4 gastric cancer cell lines were obviously lower than those in normal gastric mucosa epithelial cells (all P < 0.05). After transfection of RBMS3 overexpression vectors, RBMS3 gene was overexpressed in gastric cancer MKN-45 and SGC-7901 cells (both P < 0.05), the invasion abilities of these two cells were significantly declined (both P < 0.05). In RBMS3 gene-overexpressed MKN-45 and SGC-7901 cells, the expressions of N-cadherin and β-catenin were significantly decreased (all P < 0.05), while the expression of E-cadherin was significantly increased (both P < 0.05). After LiCl treatment, the inhibitory effect of RBMS3 on invasion of gastric cancer MKN-45 and SGC-7901 cells was partially counteracted (both P < 0.05). Conclusion: RBMS3 may inhibit the invasion and epithelial-mesenchymal transition of human gastric cancer cells by suppressing Wnt/β-catenin signal pathway. DOI:10.3781/j.issn.1000-7431.2017.11.374