The present study aimed to evaluate the underlying mechanism of microRNA-203 (miR-203) in renal cell carcinoma (RCC) involving the PI3K/AKT signaling pathway. Firstly, the functional role of miR-203 in RCC pathogenesis was determined using ectopic expression, knockdown and reporter assay experiments. The expression of miR-203, CAV1, and PI3K/AKT signaling pathway, epithelial-mesenchymal transition (EMT) and apoptosis-related genes was detected. Cell proliferation, migration, invasion and cell cycle and apoptosis were evaluated. The results revealed downregulated miR-203 and upregulated CAV1 in RCC tissues. Upregulated miR-203 and downregulated CAV1 increased E-cadherin expression and cell apoptosis, decreased β-catenin and N-cadherin expression and cell proliferation, migration and invasion, and blocked cell cycle entry. CAV1, a target gene of miR-203, decreased by up-regulated miR-203, and silencing CAV1 led to the inactivation of PI3K/AKT signaling pathway. Collectively, our findings suggested that miR-203-mediated direct suppression of CAV1 inhibits EMT of RCC cells via inactivation of the PI3K/AKT signaling pathway.
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