Silencing of the lncRNA attenuates the epithelial-mesenchymal transition of renal tubular epithelial cells by sponging via regulating β-catenin.

Renal interstitial fibrosis (RIF) is characterized by excessive extracellular matrix deposition and involves epithelial-mesenchymal transition (EMT). The lncRNA taurine-upregulated gene 1 () participates in EMT in several cancers; however, the effect and underlying mechanism of in RIF-related EMT remain unclear. Here, we explored the mechanisms by which modulates RIF. An in vivo model of renal fibrosis was established by unilateral ureteral obstruction in Balb/c mice. Human renal proximal tubular epithelial (HK-2) cells treated with transforming growth factor (TGF)-β1 were used to induce the in vitro model. Morphological changes and expression were assessed. HK-2 cells were transfected with siRNA to silence . Western blot analysis, immunofluorescence staining, cell proliferation, and migration assays were performed to examine TGF-β1-induced changes in EMT markers and EMT-like cell behaviors. and β-catenin () levels were significantly upregulated, whereas was significantly downregulated, during EMT in vitro and in vivo. knockdown or overexpression supported the epithelioid morphology of HK-2 cells while enhancing the downregulation of E-cadherin and upregulation of vimentin, α-smooth muscle actin, and β-catenin levels in TGF-β1-treated HK-2 cells. knockdown promoted the proliferation and decreased the migration of HK-2 cells and enhanced the downregulation of levels in TGF-β1-treated HK-2 cells. directly targeted , and was directly bound to . Downregulation of inhibited silencing-induced suppression of EMT. In conclusion, promotes EMT in TGF-β1-induced HK-2 cells via upregulation of β-catenin levels by sponging , suggesting a novel therapeutic candidate for RIF.