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    Recent advances reveal IL-8 signaling as a potential key to targeting breast cancer stem cells.

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    Authors
    Singh, Jagdeep K
    Simões, Bruno M
    Howell, Sacha J
    Farnie, G
    Clarke, Robert B
    Affiliation
    Breast Biology, Institute of Cancer Sciences, University of Manchester, Paterson Building, Wilmslow Road, Manchester, M20 4BX, UK. robert.clarke@manchester.ac.uk.
    Issue Date
    2013-08-30
    
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    Abstract
    Breast cancer stem-like cells (CSCs) are an important therapeutic target as they are purported to be responsible for tumor initiation, maintenance, metastases, and disease recurrence. Interleukin-8 (IL-8) is upregulated in breast cancer compared with normal breast tissue and is associated with poor prognosis. IL-8 is reported to promote breast cancer progression by increasing cell invasion, angiogenesis, and metastases and is upregulated in HER2-positive cancers. Recently, we and others have established that IL-8 via its cognate receptors, CXCR1 and CXCR2, is also involved in regulating breast CSC activity. Our work demonstrates that in metastatic breast CSCs, CXCR1/2 signals via transactivation of HER2. Given the importance of HER2 in breast cancer and in regulating CSC activity, a pathway driving the activation of these receptors would have important biological and clinical consequences, especially in tumors that express high levels of IL-8 and other CXCR1/2-activating ligands. Here, we review the IL-8 signaling pathway and the role of HER2 in maintaining an IL-8 inflammatory loop and discuss the potential of combining CXCR1/2 inhibitors with other treatments such as HER2-targeted therapy as a novel approach to eliminate CSCs and improve patient survival.
    Citation
    Recent advances reveal IL-8 signaling as a potential key to targeting breast cancer stem cells. 2013, 15 (4):210 Breast Cancer Res.
    Journal
    Breast Cancer Research
    URI
    http://hdl.handle.net/10541/304677
    DOI
    10.1186/bcr3436
    PubMed ID
    24041156
    Type
    Article
    Language
    en
    ISSN
    1465-542X
    ae974a485f413a2113503eed53cd6c53
    10.1186/bcr3436
    Scopus Count
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