Src is activated by the nuclear receptor peroxisome proliferator-activated receptor β/δ in ultraviolet

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Updated: May 6, 2026

Stimulation of Stem Cell Niches and Tissue Regeneration in Mouse Skin by Switchable Protoporphyrin IX-Dependent Photogeneration of Reactive Oxygen Species In Situ
10:05

Stimulation of Stem Cell Niches and Tissue Regeneration in Mouse Skin by Switchable Protoporphyrin IX-Dependent Photogeneration of Reactive Oxygen Species In Situ

Published on: May 8, 2020

1.8K

Alexandra Montagner, Maria B Delgado, Corinne Tallichet-Blanc

    EMBO Molecular Medicine
    |November 9, 2013
    PubMed

    Insights

    Researchers discovered a pathway involving peroxisome proliferator-activated receptor (PPAR) β/δ and the Src oncogene in UV-induced skin cancer. Targeting PPARβ/δ may offer new strategies for treating epithelial cancers.

    Area of Science:

    • Oncology
    • Molecular Biology
    • Dermatology

    Background:

    • Non-melanoma skin cancer (NMSC) is the most common human cancer with rising global incidence.
    • Mechanisms driving NMSC development are not fully understood.
    • Ultraviolet (UV) radiation is a primary risk factor for skin cancer.

    Purpose of the Study:

    • To elucidate the molecular mechanisms underlying UV-induced skin cancer development.
    • To investigate the role of peroxisome proliferator-activated receptor (PPAR) β/δ and the Src oncogene in skin carcinogenesis.
    • To explore potential therapeutic targets for epithelial cancers.

    Main Methods:

    • Utilized mouse models of UV-induced skin cancer.
    • Investigated the activity of PPARβ/δ and Src signaling pathways.
    • Assessed epithelial-to-mesenchymal transition (EMT) markers.
    • Examined human skin squamous cell carcinoma (SCC) and other epithelial cancers.
    • Employed linear models to analyze gene expression interactions.

    Main Results:

    • UV exposure activates PPARβ/δ, which directly upregulates Src expression and kinase activity.
    • Activated Src enhances the EGFR/Erk1/2 pathway, promoting EMT marker expression.
    • PPARβ/δ-deficient mice exhibited reduced skin tumor formation.
    • A PPARβ/δ antagonist inhibited UV-dependent Src activation.
    • PPARβ/δ expression positively correlated with SRC and EMT markers in human SCC.
    • Identified an interaction between PPARβ/δ, SRC, and TGFβ1 in human epithelial cancers.

    Conclusions:

    • A signaling cascade involving UV-induced PPARβ/δ and Src promotes skin cancer development.
    • PPARβ/δ plays a critical role in UV carcinogenesis and EMT.
    • Findings suggest PPARβ/δ modulators as potential therapeutic agents for various epithelial cancers.
    • The identified pathway highlights a potential therapeutic strategy for NMSC and other epithelial malignancies.

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