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    TrkA interacts with and phosphorylates STAT3 to enhance gene transcription and promote breast cancer stem cells in triple-negative and HER2-enriched breast cancers

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    Author
    Regua, Angelina T.
    Aguayo, Noah R.
    Jalboush, Sara Abu
    Doheny, Daniel L.
    Manore, Sara G.
    Zhu, Dongqin
    Wong, Grace L.
    Arrigo, Austin
    Wagner, Calvin J.
    Yu, Yang
    Thomas, Alexandra
    Chan, Michael D.
    Ruiz, Jimmy
    Jin, Guangxu
    Strowd, Roy
    Sun, Peiqing
    Lin, Jiayuh
    Lo, Hui Wen
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    Date
    2021-05-02
    Journal
    Cancers
    Publisher
    MDPI AG
    Type
    Article
    
    Metadata
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    See at
    https://doi.org/10.3390/cancers13102340
    Abstract
    JAK2–STAT3 and TrkA signaling pathways have been separately implicated in aggressive breast cancers; however, whether they are co-activated or undergo functional interaction has not been thoroughly investigated. Herein we report, for the first time that STAT3 and TrkA are significantly co-overexpressed and co-activated in triple-negative breast cancer (TNBC) and HER2-en-riched breast cancer, as shown by immunohistochemical staining and data mining. Through immu-nofluorescence staining–confocal microscopy and immunoprecipitation–Western blotting, we found that TrkA and STAT3 co-localize and physically interact in the cytoplasm, and the interaction is dependent on STAT3-Y705 phosphorylation. TrkA–STAT3 interaction leads to STAT3 phosphor-ylation at Y705 by TrkA in breast cancer cells and cell-free kinase assays, indicating that STAT3 is a novel substrate of TrkA. β-NGF-mediated TrkA activation induces TrkA–STAT3 interaction, STAT3 nuclear transport and transcriptional activity, and the expression of STAT3 target genes, SOX2 and MYC. The co-activation of both pathways promotes breast cancer stem cells. Finally, we found that. © 2021 by the authors.
    Sponsors
    U.S. Department of Defense
    Keyword
    Breast cancer
    Cancer stem cells
    MYC
    SOX2
    STAT3
    TrkA
    Identifier to cite or link to this item
    http://hdl.handle.net/10713/15716
    ae974a485f413a2113503eed53cd6c53
    10.3390/cancers13102340
    Scopus Count
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