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    Survival of head and neck cancer cells relies upon LZK Kinase-mediated stabilization of mutant p53

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    Authors
    Edwards, Zoe C
    Trotter, Eleanor W
    Torres-Ayuso, Pedro
    Chapman, Phil
    Wood, H
    Nyswaner, Katherine
    Brognard, John
    Affiliation
    Signalling Networks in Cancer, Cancer Research UK Manchester Institute
    Issue Date
    2017-07-31
    
    Metadata
    Show full item record
    Abstract
    Head and neck squamous cell carcinoma (HNSCC) includes epithelial cancers of the oral and nasal cavity, larynx, and pharynx and accounts for ∼350,000 deaths per year worldwide. Smoking-related HNSCC is associated with few targetable mutations but is defined by frequent copy-number alteration, the most common of which is gain at 3q. Critical 3q target genes have not been conclusively determined for HNSCC. Here, we present data indicating that MAP3K13 (encoding LZK) is an amplified driver gene in HNSCC. Copy-number gain at 3q resulted in increased MAP3K13 mRNA in HNSCC tumor samples and cell lines. Silencing LZK reduced cell viability and proliferation of HNSCC cells with 3q gain but not control cell lines. Inducible silencing of LZK caused near-complete loss of colony-forming ability in cells harboring 3q gain. These results were validated in vivo by evidence that LZK silencing was sufficient to reduce tumor growth in a xenograft model of HNSCC. Our results establish LZK as critical for maintaining expression of mutant stabilized p53. Cancer Res; 1-12. ©2017 AACR.
    Citation
    Survival of head and neck cancer cells relies upon LZK Kinase-mediated stabilization of mutant p53. 2017 Cancer Res.
    Journal
    Cancer Research
    URI
    http://hdl.handle.net/10541/620554
    DOI
    10.1158/0008-5472.CAN-17-0267
    PubMed ID
    28760853
    Type
    Article
    Language
    en
    ISSN
    1538-7445
    ae974a485f413a2113503eed53cd6c53
    10.1158/0008-5472.CAN-17-0267
    Scopus Count
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    All Paterson Institute for Cancer Research

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