miRNA-204-5p acts as a tumor suppressor in gastric cancer by inhibiting cell migration, invasion, and glycolysis via the RAB22A/PI3K/AKT axis.

Gastric cancer (GC) is a highly prevalent and lethal malignancy worldwide. Accumulating evidence has shown that microRNAs (miRNAs) play essential roles in the development and progression of GC. In this study, we aimed to investigate the expression, functions, and molecular mechanisms of miRNA-204-5p in GC. We found that miRNA-204-5p was significantly downregulated in GC cell lines compared to their normal counterparts. Functional experiments demonstrated that miRNA-204-5p inhibited the migration, invasion, and glycolysis of GC cells in vitro and suppressed tumor lung metastasis in vivo. Mechanistically, miRNA-204-5p exerted its tumor-suppressive effects by directly targeting RAB22A and inhibiting the PI3K/AKT signaling pathway. Overexpression of RAB22A partially reversed the inhibitory effects of miRNA-204-5p on the malignant phenotypes and the PI3K/AKT pathway activation in GC cells. Furthermore, miRNA-204-5p regulated the expression of molecules related to epithelial-mesenchymal transition, and glycolysis through the RAB22A/PI3K/AKT axis. Our findings suggest that miRNA-204-5p functions as a tumor suppressor in GC by targeting RAB22A and provide novel insights into the molecular mechanisms underlying GC progression. The miRNA-204-5p/RAB22A axis may serve as a potential diagnostic biomarker and therapeutic target for GC.