MicroRNA-708 represses hepatic stellate cells activation and proliferation by targeting ZEB1 through Wnt/β-catenin

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Junfa Yang1, Qing Tao2, Yiwen Zhou3

  • 1Key Laboratory of Anti-inflammatory and Immune Medicine, Ministry of Education, Institute of Clinical Pharmacology, Anhui Medical University, Hefei, China; School of Pharmacy, Anhui Medical University, Hefei, 230032, China; The Key Laboratory of Anti-inflammatory and Immune Medicines, Ministry of Education, Anhui Medical University, Hefei, 230032, China; Anhui Province Key Laboratory of Major Autoimmune Diseases, Anhui Institute of Innovative Drugs, Hefei, 230032, China.

European Journal of Pharmacology
|January 22, 2020
PubMed

Insights

MicroRNA-708 (miR-708) suppresses liver fibrosis by inhibiting hepatic stellate cell activation. This study reveals miR-708 targets ZEB1, offering a potential therapeutic strategy for liver fibrosis.

Area of Science:

  • Hepatology
  • Molecular Biology
  • Cell Biology

Background:

  • Liver fibrosis results from chronic liver injury and hepatic stellate cell (HSC) activation.
  • MicroRNAs (miRNAs) regulate biological processes, with miR-708 known to inhibit hepatocellular carcinoma.
  • The role of miR-708 in liver fibrosis remains largely unexplored.

Purpose of the Study:

  • To investigate the role of miR-708 in liver fibrosis.
  • To determine if miR-708 regulates HSC activation and proliferation.
  • To identify the molecular targets of miR-708 in the context of liver fibrosis.

Main Methods:

  • Quantitative real-time PCR to measure miR-708 and ZEB1 expression in fibrotic liver tissues and HSCs.
  • Cell proliferation and activation assays using LX-2 cells with miR-708 overexpression or knockdown, and ZEB1 silencing or overexpression.
  • Dual-luciferase reporter assays to confirm direct targeting of ZEB1 by miR-708.
  • Western blotting and Wnt/β-catenin pathway analysis.

Main Results:

  • miR-708 expression was significantly decreased in fibrotic liver tissues and activated HSCs.
  • ZEB1 expression was inversely correlated with miR-708 levels.
  • Overexpression of miR-708 or silencing of ZEB1 inhibited HSC activation and proliferation.
  • miR-708 directly targets ZEB1, and ZEB1 regulates HSCs via the Wnt/β-catenin pathway.

Conclusions:

  • miR-708 acts as a tumor suppressor in liver fibrosis by targeting ZEB1.
  • Modulating miR-708 levels may represent a novel therapeutic approach for liver fibrosis.
  • The miR-708/ZEB1 axis plays a critical role in HSC activation and liver fibrogenesis.
Keywords:
Hepatic stellate cellsMiR-708MicroRNAZEB1liver fibrosis

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