Livin is involved in TGF-β1-induced renal tubular epithelial-mesenchymal transition through lncRNA-ATB

Abstract

Background Renal interstitial fibrosis is accepted as a crucial component of chronic kidney diseases (CKD). Epithelial-mesenchymal transition (EMT) is an important factor contributing to renal interstitial fibrosis. Livin, due to its ability to induce EMT, is an important regulator of many types of tumors and might also be involved in human renal tubular EMT. Methods We confirmed that Livin and lncRNA-ATB could aggravate EMT in vivo and in vitro, lncRNA-ATB could be suppressed by the silencing of Livin whereas Livin expression was nearly stable when lncRNA-ATB was overexpressed or knocked out. Results Livin was upregulated in vivo and in vitro at the similar rate as the occurrence of EMT, which could be relieved when Livin was silenced. LncRNA-ATB, which is another important regulator of EMT, was also found highly expressed during this process. The silencing of lncRNA-ATB could lessen the severity of EMT, and the overexpression of lncRNA-ATB could aggravate EMT without affecting the expression of Livin. Conclusions Livin promotes EMT through the regulation of lncRNA-ATB. The silencing of Livin might be an effective targeted therapy for renal fibrosis.