Suppressed the Progression of the Clear Cell Renal Cell Carcinoma by Targeting Gene Expression.

Clear cell renal cell carcinoma (ccRCC) is a malignant tumor of kidney epithelial cells, one of the most common tumors in the world. Transforming growth factor beta (TGFβ)1 is a crucial factor that induces epithelial-mesenchymal transition (EMT) in cancer cells. is a microRNA that is considered a tumor suppressor. However, the role and mechanism of in TGFβ1-induced ccRCC cells are not fully understood. This study investigated the roles of and its target gene in regulating EMT in ccRCC development. 786-0 and Caki-1cells were treated with TGFβ1 to induce EMT. The levels of and TGFβ2 were determined by quantitative real-time polymerase chain reaction and Western blotting. The progression of EMT was evaluated by E-cadherin detection by immunofluorescence, and E-cadherin, N-cadherin, and vimentin detection by Western blotting. Furthermore, migration and invasion capacities were assessed using a Transwell system. The direct binding of with the target gene was confirmed by dual luciferase reporter gene assay. Results indicated that TGFβ1 treatment decreased the protein abundance of E-cadherin while increasing the protein expression of N-cadherin and vimentin, indicating TGFβ1-induced EMT was constructed successfully. Moreover, TGFβ1 treatment repressed the expression of . mimics reversed the effect of TGFβ1 on the migration, invasion, and expression of E-cadherin, N-cadherin, and vimentin. The directly binds with the 3' untranslated region of mRNA and suppresses its expression. Furthermore, TGFβ2 overexpression abrogated the above changes regulated by mimics. Taken together, inhibited TGFβ1-induced EMT by suppressing the migration and invasion of ccRCC cells via directly targeting gene expression.