CRNDE mediates the viability and epithelial-mesenchymal transition of renal cell carcinoma via miR-136-5p.

Long non-coding RNAs (lncRNAs) regulate epithelial-mesenchymal transition (EMT) and the mutual adhesion and development of renal cell carcinoma (RCC). The underlying molecular mechanism of EMT and RCC cells in the treatment of RCC was less reported. In this study, the related functional lncRNA and miRNA in RCC tissues were predicted by bioinformatics analysis and verified by quantitative real-time PCR (qRT-PCR). The RNA interference technology was applied to measure the effects of the predicted lncRNAs and miRNAs on RCC cells. The expressions of EMT-related mRNAs and proteins were determined using qRT-PCR and Western-blot experiments. CRNDE was overexpressed and miR-136-5p was low-expressed in RCC. Upregulation of CRNDE could promote the viability, migration, invasion of RCC, while downregulation of CRNDE produced the opposite effects. Both the upregulation and downregulation of CRNDE alternated the protein expressions related to EMT, while miR-136-5p resulted in the opposite effects on CRNDE. Moreover, the promotive effect of overexpressed CRNDE on RCC cells could be blocked by miR-136-5p mimic. CRNDE can mediate miR-136-5p, promote the development of EMT and RCC cells, showing the potential to serve as a novel biomarker and therapeutic target in RCC treatment.