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Current Perspective| Volume 64, P96-100, September 2016

Can Wnt5a and Wnt non-canonical pathways really mediate adipocyte de-differentiation in a tumour microenvironment?

      Highlights

      • Trans-differentiation of adipose tissue to mesenchymal cells is a fundamental issue in oncology and translational medicine.
      • The role of Wnt5a in adipocyte de-differentiation should be reappraised and reviewed.
      • De-differentiation of peritumoural adipose tissue may derive from the beta-catenin pathway of Wnt10b.
      • Targeting Wnt5a for pancreas cancer therapy needs further research to be assessed.

      Abstract

      Wnt5a has been recently reported as a possible triggering factor of adipocyte de-differentiation into an adipocyte-derived fibroblast in the tumour microenvironment of pancreas cancer. The Wnt/β-catenin pathway was described in processes involving de-differentiation and epithelial-mesenchymal transition but some Wnt family-belonging molecules exert an adipogenic role on adipocyte, while other ones, such as Wnt10b or Wnt3a, an anti-adipogenic role. Although this ability depends on the different tumoural microenvironments, it is intriguing to ascertain if some Wnt molecules, participating in the non-canonical pathway, may be targeted as fundamental factors able to trigger the desmoplastic reaction of peritumoural white adipose tissue.

      Keywords

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