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.

较长的非编码RNA（lncRNA）调节上皮-间质转化（EMT）以及肾细胞癌的相互粘附和发展（RCC）。EMT和RCC细胞在RCC治疗中的潜在分子机制报道较少。在这项研究中，通过生物信息学分析预测了RCC组织中的相关功能lncRNA和miRNA，并通过定量实时PCR（qRT-PCR）进行了验证。RNA干扰技术用于测量预测的lncRNA和miRNA对RCC细胞的作用。使用qRT-PCR和Western-blot实验确定EMT相关mRNA和蛋白的表达。在RCC中CRNDE过表达，而miR-136-5p低表达。CRNDE的上调可以促进RCC的活力，迁移，侵袭，而CRNDE的下调则产生相反的作用。CRNDE的上调和下调都交替了与EMT相关的蛋白质表达，而miR-136-5p对CRNDE产生相反的作用。此外，miR-136-5p模拟物可以阻止过度表达的CRNDE对RCC细胞的促进作用。CRNDE可以介导miR-136-5p，促进EMT和RCC细胞的发育，显示出在RCC治疗中作为新型生物标志物和治疗靶标的潜力。