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Effects of Wnt-1 blockade in DEN-induced hepatocellular adenomas of mice

Argyrios Sklavos1, Theofilos Poutahidis2, Alexander Giakoustidis3

  • 1Division of Transplant Surgery, Department of Surgery, School of Medicine, Faculty of Health Sciences, Aristotle University and Hippokration General Hospital, Thessaloniki 54642, Greece.

Oncology Letters
|February 6, 2018
PubMed

Insights

Blocking Wnt-1 signaling in mice with hepatocellular carcinoma (HCC) suppressed key pathway elements and proliferation markers. However, Wnt-1 blockade did not affect tumor size or multiplicity, indicating apoptosis is crucial for counteracting HCC.

Area of Science:

  • Oncology
  • Molecular Biology
  • Hepatology

Background:

  • The Wnt/β-catenin signaling pathway plays a role in hepatocellular carcinoma (HCC) development and growth.
  • Targeting this pathway is a potential strategy for anti-HCC therapies.

Purpose of the Study:

  • To investigate the effects of Wnt-1 blockade on HCC using a chemical carcinogenesis mouse model.
  • To assess the impact of Wnt-1 blockade on Wnt/β-catenin signaling pathway components and hepatocellular adenomas.

Main Methods:

  • Utilized the diethylnitrosamine (DEN)-induced chemical carcinogenesis mouse model of HCC.
  • Administered neutralizing anti-Wnt-1 antisera for ten consecutive days to 9-month-old mice.
  • Examined mice for 20 days post-treatment, analyzing hepatocellular adenomas and serum markers.

Main Results:

  • Wnt-1 blockade suppressed key Wnt/β-catenin pathway elements (β-catenin, Frizzled-1 receptor) but not Dickkopf-related protein 1.
  • Suppressed expression of proliferation markers (Cyclin D1, FOXM1, NF-κΒ, c-Jun) and apoptosis regulator (Bcl-2).
  • Serum levels of c-Met were reduced; however, tumor size and multiplicity remained unaffected.

Conclusions:

  • Wnt-1 blockade effectively inhibits critical components of the Wnt/β-catenin pathway and proliferation markers in DEN-induced HCC.
  • Despite suppressing proliferation, Wnt-1 blockade did not alter tumor burden, suggesting apoptosis plays an equally important role in counteracting HCC development.
Keywords:
Wnt-1diethylnitrosaminehepatocellular cancermiceβ-catenin

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