Up-regulation of E-cadherin by saRNA inhibits the migration and invasion of renal carcinoma cells

Previous studies have reported that double stranded RNAs (dsRNAs) have a potent ability to induce gene expression by targeting its promoter in cancer cells, which is called RNA activation (RNAa). In the present study, we have identified that a candidate dsRNA (dsEcad-215) could stimulate E-cadherin mRNA and protein expression via RNAa in renal cell carcinoma (RCC). Because the expression level of E-cadherin was down-regulated in RCC tissues compared to adjacent non-tumor tissues, dsEcad-215 was subsequently transfected into the RCC cell lines ACHN and 786-O. Expectedly, our results indicated that transfection of dsEcad-215 readily inhibited cell migration and invasion. In addition, several critical EMT-promoting genes (ZEB-1 and Vimentin) were down-regulated, while the anti-EMT gene β-catenin was up-regulated both at the mRNA and protein levels after dsEcad-215 transfection, suggesting that an enhanced E-cadherin level by dsEcad-215 suppressed EMT to inhibit cell motility. Collectively, our findings provide a potential effective therapeutic strategy for RCC, and dsEcad-215 might act as an alternative anti-cancer metastasis drug.