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Functional expression of TWEAK in human hepatocellular carcinoma: possible implication in cell proliferation and

Tomoyuki Kawakita1, Katsuya Shiraki, Yutaka Yamanaka

  • 1First Department of Internal Medicine, Mie University School of Medicine, Tsu, Mie 514-8507, Japan.

Biochemical and Biophysical Research Communications
|May 18, 2004
PubMed

Insights

TNF-like weak inducer of apoptosis (TWEAK) promotes hepatocellular carcinoma (HCC) cell proliferation via autocrine and paracrine signaling. TWEAK also influences tumor angiogenesis by affecting endothelial cells.

Area of Science:

  • Oncology
  • Cell Biology
  • Immunology

Background:

  • TNF-like weak inducer of apoptosis (TWEAK) is a TNF family member with diverse biological activities.
  • TWEAK expression is observed in various human tissues.
  • The role of TWEAK in human hepatocellular carcinomas (HCCs) requires further investigation.

Purpose of the Study:

  • To investigate TWEAK sensitivity, expression, and its physiological role in human HCCs.
  • To determine TWEAK's impact on HCC cell proliferation and signaling pathways.
  • To assess TWEAK's influence on tumor-related angiogenesis.

Main Methods:

  • Detection of TWEAK receptor in HCC cell lines.
  • Assessment of TWEAK's effect on HCC cell proliferation and NF-κB activation.
  • Evaluation of TWEAK's role in human umbilical vein endothelial cell (HUVEC) proliferation, IL-8, and MCP-1 secretion.
  • Inhibition of HUVEC tube formation using anti-TWEAK antibody.

Main Results:

  • TWEAK receptor was detected in four HCC cell lines.
  • TWEAK significantly promoted HCC cell proliferation and induced NF-κB activation.
  • HCC cells constitutively express TWEAK, with soluble TWEAK detected in culture medium.
  • TWEAK promoted HUVEC proliferation and induced IL-8 and MCP-1 secretion.
  • Anti-TWEAK antibody inhibited endothelial cell tube formation.

Conclusions:

  • TWEAK plays a critical role in HCC cellular proliferation through autocrine and paracrine mechanisms.
  • TWEAK modulates tumor-related angiogenesis by affecting endothelial cells.
  • Targeting TWEAK may offer a therapeutic strategy for HCC.

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