miR-205 suppresses cell proliferation, invasion, and metastasis via regulation of the PTEN/AKT pathway in renal cell carcinoma

The present study aimed to determine the importance of microRNA-205 (miR-205) in the proliferation, apoptosis, invasion and metastasis of renal cell carcinoma (RCC) cells and the underlying molecular mechanisms. Reverse transcription-polymerase chain reaction was used to quantify the expression levels of miR-205 in RCC tissue, normal tissue adjacent to carcinoma, RCC cells and normal renal cells. It was determined that the expression levels of miR-205 in RCC tissue and cells were reduced compared with those in normal tissue and renal cells. miR-205 mimics and the negative control were prepared and transfected into RCC cells. Cell viability and apoptosis were investigated using methyl thiazolyl tetrazolium assay and Annexin V-fluorescein isothiocyanate/propidium iodide staining, respectively. Cell migration and invasion were evaluated with Transwell assays. The protein expression levels of E2F transcription factor 1 (E2F1), B-cell lymphoma-2 (Bcl-2), E-cadherin, vimentin, phosphatase and tensin homolog (PTEN) and phosphorylated AKT serine/threonine kinase 1 (p-AKT) were determined with western blot analysis. It was revealed that miR-205 promoted the apoptosis of RCC cells and suppressed their proliferation, metastasis and invasion compared with the negative control. The expression levels of E2F1, Bcl-2, vimentin and p-AKT were downregulated compared with the negative control. The expression levels of E-cadherin and PTEN were upregulated in the cells transfected with miR-205 mimics compared with the negative control group. Therefore, it was concluded that miR-205 suppressed cell proliferation, invasion, and metastasis in RCC cells via regulation of the PTEN/AKT signaling pathway. The present study may contribute to future miRNA-based RCC therapy.