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TM4SF5-Mediated Roles in the Development of Fibrotic Phenotypes

Jihye Ryu1, Jung Weon Lee1

  • 1Department of Pharmacy, Research Institute of Pharmaceutical Sciences, Tumor Microenvironment Global Core Research Center, Medicinal Bioconvergence Research Center, College of Pharmacy, Seoul National University, Seoul 08826, Republic of Korea.

Mediators of Inflammation
|May 2, 2017
PubMed

Insights

Transmembrane 4 L six family member 5 (TM4SF5) drives liver fibrosis by regulating cell growth and extracellular matrix. Targeting TM4SF5 with specific compounds or antibodies shows promise in reducing fibrotic phenotypes.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Hepatology

Background:

  • Transmembrane 4 L six family member 5 (TM4SF5) forms tetraspanin-enriched microdomains (TERMs) on cell surfaces.
  • TERMs regulate intercellular communication and control diverse cellular functions, including epithelial-mesenchymal transition (EMT) and metastasis.
  • TM4SF5 is implicated in various cellular processes, including aberrant growth, drug resistance, and migration.

Purpose of the Study:

  • To review current data on the role of TM4SF5 in the development of fibrotic phenotypes.
  • To discuss the molecular mechanisms by which TM4SF5 contributes to liver fibrosis.
  • To explore antifibrotic strategies targeting TM4SF5 and its associated signaling networks.

Main Methods:

  • Review of existing literature on TM4SF5 and fibrotic phenotypes.
  • Analysis of TM4SF5 induction by transforming growth factor β1 (TGFβ1) and epidermal growth factor receptor (EGFR) signaling.
  • Investigation of TM4SF5's role in hepatocyte cell cycle, migration, and extracellular matrix production.
  • Examination of TM4SF5, α-smooth muscle actin (α-SMA), and collagen I expression in CCl4-treated mice.

Main Results:

  • TM4SF5 expression is induced by TGFβ1 and EGFR activation.
  • In hepatocytes, TM4SF5 regulates cell cycle, migration, and extracellular matrix component expression.
  • TM4SF5, α-SMA, and collagen I are co-expressed in fibrotic liver septa of CCl4-treated mice.
  • Antifibrotic reagents targeting TM4SF5 diminish fibrotic phenotypes.

Conclusions:

  • TM4SF5 plays a significant role in the development of liver fibrosis.
  • Targeting TM4SF5 and its associated protein networks offers a potential therapeutic strategy for liver fibrosis.
  • Specific small compounds and chimeric antibodies against TM4SF5 demonstrate antifibrotic effects.

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