Abstract Objectives Renal fibrosis (RF) is a critical pathway in the progression of chronic kidney disease (CKD) to end-stage kidney diseases. This study aimed to investigate the role of miR-101-3p in the progression of fibrosis in renal tubular epithelial cells (RTECs) and to elucidate the underlying molecular mechanisms. Methods An RF cell model was established by induction with transforming growth factor-β1 (TGF-β1). The expression levels of miR-101-3p and fibrosis-associated proteins were measured using quantitative real-time reverse transcription polymerase chain reaction. Cell migration ability was detected by Transwell assay. The potential target genes of miR-101-3p were predicted through bioinformatic analysis. The interaction between miR-101-3p and EZH2 was verified using the luciferase assay and RNA immunoprecipitation (RIP) assay. Results HK-2 cells treated with TGF-β1 showed downregulated expression of miR-101-3p. Overexpression of miR-101-3p reduced cell migration and decreased the production of fibronectin, collagen IV and α-smooth muscle actin (α-SMA). EZH2 was identified as a downstream target gene of miR-101-3p. The interaction between miR-101-3p and EZH2 was confirmed by luciferase assay and RIP assay. EZH2 was upregulated in TGF-β1-induced cells. Upregulation of EZH2 partially reversed the anti-fibrotic effects caused by miR-101-3p overexpression. Conclusions miR-101-3p alleviates TGF-β1-induced fibrosis in RTECs by inhibiting EZH2. This study provides new insights into the molecular mechanisms of RF and suggests potential therapeutic targets for CKD.
Xu et al. (Fri,) studied this question.
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