Fibrotic Enzymes Modulate Wound-Induced Skin Tumorigenesis

    March 2021 in “ EMBO Reports ”
    Lisette Van Hove, Kim Lecomte, Jana Roels, Niels Vandamme, Hanna‐Kaisa Vikkula, Isabelle Hoorens, Katia Ongenae, Tino Hochepied, Giacomo Donati, Yvan Saeys, Sven Quist, Fiona M. Watt, Geert Loo, Esther Hoste
    TLDR PRSS35 enzyme may help start skin tumors and could be a target for cancer treatment.
    The study explored the role of the enzyme PRSS35 in wound-induced skin tumorigenesis, revealing that cancer-associated fibroblasts (CAFs) in these tumors exhibited a fibrotic gene signature with high PRSS35 expression. Deleting PRSS35 in mice led to abnormal collagen composition and increased tumor incidence, suggesting its role in regulating tumor initiation by remodeling the extracellular matrix (ECM). PRSS35 was also upregulated in high-grade human squamous cell carcinomas, indicating its potential as a biomarker for tumor staging. The findings highlighted the importance of fibrotic responses in cancer progression and suggested PRSS35 as a potential therapeutic target.
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