miR-1294 alleviates epithelial-mesenchymal transition by repressing FOXK1 in gastric cancer

Background MicroRNAs (miRNAs) have been reported play critical roles in regulating tumor development and progression. Objective This study aimed to investigate the potential effect of miR-1294 in gastric cancer (GC). Methods Reverse transcription quantitative polymerase chain reaction (RT-PCR) were performed to verify the expression level of miR-1294 and Forkhead box protein K1 (FOXK1). Overall survival data of miR-1294 for GC was analysed by log-rank test. Targetscan was used to screen potential target gene of miR-1294. Dual luciferase assay was assessed to investigate the relationship between miR-1294 and FOXK1. The miR-1294 overexpression and knockdown were designed to study the biological function of miR-1294. The migration and invasion of GC cell lines were investigated by wound healing and transwell assays. Western blotting were performed to verify the expression level of epithelial marker, mesenchymal markers and FOXK1. Overexpression of FOXK1 was designed to study the rescue effects of FOXK1 in SGC7901 cell. Results miR-1294 was found downregulated in GC patients and cell lines. A higher miR-1294 expression showed a significant longer overall survival than those with a lower miR-1294 expression. miR-1294 directly targets FOXK1 and regulates the expression of FOXK1. In addition, miR-1294 regulates epithelial-mesenchymal transition (EMT) by inhibiting FOXK1 in GC cells and it can be rescued by overexpression of FOXK1. Conclusion miR-1294 alleviates EMT process in GC by targeting FOXK1.