Titre
Nuclear receptor peroxisome proliferator activated receptor (PPAR) beta/delta in skin wound healing and cancer
Type
synthèse (review)
Institution
UNIL/CHUV/Unisanté + institutions partenaires
Périodique
Auteur(s)
Montagner, A.
Auteure/Auteur
Wahli, W.
Auteure/Auteur
Tan, N.S.
Auteure/Auteur
Liens vers les personnes
Liens vers les unités
ISSN
1952-4013
Statut éditorial
Publié
Date de publication
2015
Volume
25
Numéro
Suppl 1
Première page
4
Dernière page/numéro d’article
11
Langue
anglais
Résumé
We review the functions of peroxisome proliferator activated receptor (PPAR) beta/delta in skin wound healing and cancer. In particular, we highlight the roles of PPAR beta/delta in inhibiting keratinocyte apoptosis at wound edges via activation of the PI3K/PKB alpha/Akt1 pathway and its role during re-epithelialization in regulating keratinocyte adhesion and migration. In fibroblasts, PPAR beta/delta controls IL-1 signalling and thereby contributes to the homeostatic control of keratinocyte proliferation. We discuss its therapeutic potential for treating diabetic wounds and inflammatory skin diseases such as psoriasis and acne vulgaris. PPAR beta/delta is classified as a tumour growth modifier; it is activated by chronic low-grade inflammation, which promotes the production of lipids that, in turn, enhance PPAR beta/delta transcription activity. Our earlier,work unveiled a cascade of events triggered by PPAR beta/delta that involve the oncogene Src, which promotes ultraviolet-induced skin cancer in mice via enhanced EGFR/Erk1/2 signalling and the expression of epithelial-to-mesenchymal transition (EMT) markers. Interestingly, PPAR beta/delta expression is correlated with the expression of SRC and EMT markers in human skin squamous cell carcinoma. Furthermore, there is a positive interaction between PPAR beta/delta, SRC, and TGF beta 1 at the transcriptional level in various human epithelial cancers. Taken together, these observations suggest the need for evaluating PPAR beta/delta modulators that attenuate or increase its activity, depending on the therapeutic target.
PID Serval
serval:BIB_FE7C0A4E7D5B
Date de création
2015-08-13T13:08:22.926Z
Date de création dans IRIS
2025-05-21T07:24:59Z