miR-630 inhibits epithelial-to-mesenchymal transition (EMT) by regulating Wnt/betacatenin pathway in gastric cancer cells.

Despite availability of different treatments, gastric cancer remains the second highest cause of cancer-related deaths worldwide. This study was aimed to explore the role of miR-630 in gastric cancer by investigating the underlying mechanism of inhibiting epithelial-to-mcsenchymal transition (EMT) of SGC-7901 and BGC-823 cells through the Wnt/beta-catenin pathway. Results showed that miR-630 was downregulated in several gastric cancer cell lines, including SGC-7901 and BGC-823. Transfection of miR-630 mimic showed a significant decrease in wound healing in a scratch assay in both cell lines compared to a scramble group. Also, transfection of miR-630 mimic inhibited cell viability, migration, and invasion of gastric cancer cells. miR-630 mimic transfection suppressed EMT by activating the Wnt/beta-catenin pathway. This was supported by the fact that miR-630-mediated suppression of the EMT phenotype was reversed in the presence of the Wnt/beta-catenin inhibitor ICG001. miR-630 plays a protective role against gastric cancer by suppressing EMT through activating the Wnt/beta-catenin pathway.