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Blocking Wnt as a therapeutic target in mice model of skin cancer

Abdullah Alyoussef1, Medhat Taha2

  • 1Department of Internal Medicine (Dermatology), Faculty of Medicine, University of Tabuk, Tabuk, 71471, Saudi Arabia. aalyoussef@ut.edu.sa.

Archives of Dermatological Research
|June 6, 2019
PubMed

Insights

Blocking the Wnt pathway with IWP12 effectively treats skin cancer in mice. This approach reduces inflammation and fibrosis by modulating key signaling molecules and cytokines, offering a promising therapeutic strategy.

Area of Science:

  • Oncology
  • Molecular Biology
  • Dermatology

Background:

  • The Wnt pathway is crucial for cancer cell metabolism, promoting inflammation via NFκB and fibrosis via TGF-β.
  • Targeting the Wnt pathway presents a potential therapeutic strategy for various cancers.

Purpose of the Study:

  • To investigate the therapeutic effects of blocking the Wnt pathway using IWP12 in a mouse model of skin cancer.
  • To assess the impact of IWP12 on skin cancer-induced inflammation and fibrosis.

Main Methods:

  • Skin cancer was induced in mice using 7,12-dimethylbenz[a]anthracene (DMBA) and croton oil.
  • Gene and protein expression of Wnt signaling components, inflammatory markers (NFκB, TNF-α), and fibrotic markers (SMAD, TGF-β) were analyzed.
  • Histopathological analysis using hematoxylin/eosin staining evaluated skin tissue structure.

Main Results:

  • IWP12 treatment completely blocked Wnt signaling in skin cancer mice without affecting controls.
  • IWP12 significantly attenuated skin hyperkeratosis, parakeratosis, acanthosis, and dysplasia.
  • IWP12 reduced the expression of β-catenin, SMAD, TGF-β, NFκB, and TNF-α, while increasing IL-4 and IL-10 expression.

Conclusions:

  • Blocking Wnt pathway activation with IWP12 ameliorates skin cancer by inhibiting pro-inflammatory cytokines and enhancing anti-inflammatory cytokines.
  • IWP12 treatment effectively reduces skin cancer-induced inflammation and fibrosis, demonstrating its therapeutic potential.
Keywords:
Interleukin (IL)-4/10Nuclear factor (NF)κBTransforming growth factor (TGF)-βTumor necrosis factor (TNF)-αWntβ-Catenin

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