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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Article info
Publication history
Published online: July 05, 2016
Accepted:
May 25,
2016
Received in revised form:
May 7,
2016
Received:
March 29,
2016
Identification
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© 2016 Elsevier Ltd. All rights reserved.