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Updated: Oct 22, 2025

Studying TGF-β Signaling and TGF-β-induced Epithelial-to-mesenchymal Transition in Breast Cancer and Normal Cells
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Studying TGF-β Signaling and TGF-β-induced Epithelial-to-mesenchymal Transition in Breast Cancer and Normal Cells

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Noncanonical FZD2 Signaling Induces EMT and Tumor Progression

    Cancer Discovery
    |August 28, 2021
    PubMed

    Insights

    Frizzled 2 (FZD2) and WNT5A proteins promote cancer cell epithelial-mesenchymal transition (EMT) and metastasis. This occurs through a noncanonical pathway involving FYN and STAT3 signaling.

    Area of Science:

    • Molecular oncology
    • Cell signaling pathways
    • Cancer metastasis research

    Background:

    • Epithelial-mesenchymal transition (EMT) is crucial for cancer metastasis.
    • Noncanonical Wnt signaling pathways regulate various cellular processes, including EMT.

    Purpose of the Study:

    • To elucidate the molecular mechanisms by which FZD2 and WNT5A contribute to EMT and metastasis.
    • To identify key signaling molecules involved in this noncanonical pathway.

    Main Methods:

    • Investigated the roles of Frizzled 2 (FZD2) and WNT5A in cancer cell models.
    • Utilized molecular biology techniques to analyze the involvement of FYN and STAT3 signaling.

    Main Results:

    • FZD2 and WNT5A were found to activate a noncanonical pathway.
    • This pathway involves the kinases FYN and the transcription factor STAT3.
    • Activation of this pathway drives EMT and enhances metastatic potential.

    Conclusions:

    • FZD2 and WNT5A are key drivers of EMT and metastasis through a noncanonical FYN/STAT3 signaling axis.
    • Targeting this pathway may offer novel therapeutic strategies for inhibiting cancer spread.

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