The role of lncRNA-ZFAS1 in liver fibrosis: insights into the miR-1953/TAZ axis.

Abstract

Long non-coding RNA-Zinc finger antisense 1 (lncRNA-ZFAS1) is involved in the progression of several cancer types, yet its function in liver fibrosis remains unclear. The purpose of this study was to examine ZFAS1 expression in liver fibrosis and explore its possible molecular mechanism. ZFAS1 expression was measured in a liver fibrosis model and in activated hepatic stellate cells (HSCs). The impact of ZFAS1 silencing on HSC growth, collagen production, and epithelial-mesenchymal transition (EMT) was assessed. The connection between ZFAS1 and miR-1953 was investigated using bioinformatics analysis and luciferase reporter gene experiments. Moreover, in vivo studies were performed to confirm the effect of ZFAS1 knockdown on liver fibrosis progression. ZFAS1 was significantly upregulated in the liver fibrosis model and activated HSCs. Silencing ZFAS1 helped to inhibit the growth and activation of HSCs, along with reduced levels of type I collagen and α-SMA. In vivo experiments confirmed that ZFAS1 knockdown alleviated the progression of fibrosis and collagen deposition. Mechanistic studies revealed that ZFAS1 promoted HSC EMT through the regulation of the miR-1953/TAZ axis, thereby exerting a pro-fibrotic effect. By influencing the miR-1953/TAZ signaling pathway, ZFAS1 significantly contributes to the activation and EMT of HSCs in liver fibrosis development. These findings highlight ZFAS1 as a potential therapeutic target for treating liver fibrosis, offering new avenues for clinical intervention.