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    JNK suppresses tumor formation via a gene-expression program mediated by ATF2.

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    Authors
    Gozdecka, Malgorzata
    Lyons, Steve
    Kondo, S
    Taylor, J
    Li, Yaoyong
    Walczynski, J
    Thiel, G
    Breitwieser, Wolfgang
    Jones, Nic
    Affiliation
    Department of Cell Regulation, CRUK Manchester Institute, Paterson Building, University of Manchester, Manchester
    Issue Date
    2014-11-20
    
    Metadata
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    Abstract
    JNK and p38 phosphorylate a diverse set of substrates and, consequently, can act in a context-dependent manner to either promote or inhibit tumor growth. Elucidating the functions of specific substrates of JNK and p38 is therefore critical for our understanding of these kinases in cancer. ATF2 is a phosphorylation-dependent transcription factor and substrate of both JNK and p38. Here, we show ATF2 suppresses tumor formation in an orthotopic model of liver cancer and cellular transformation in vitro. Furthermore, we find that suppression of tumorigenesis by JNK requires ATF2. We identify a transcriptional program activated by JNK via ATF2 and provide examples of JNK- and ATF2-dependent genes that block cellular transformation. Significantly, we also show that ATF2-dependent gene expression is frequently downregulated in human cancers, indicating that amelioration of JNK-ATF2-mediated suppression may be a common event during tumor development.
    Citation
    JNK suppresses tumor formation via a gene-expression program mediated by ATF2. 2014, 9 (4):1361-74 Cell Rep
    Journal
    Cell Reports
    URI
    http://hdl.handle.net/10541/338677
    DOI
    10.1016/j.celrep.2014.10.043
    PubMed ID
    25456131
    Type
    Article
    Language
    en
    ISSN
    2211-1247
    ae974a485f413a2113503eed53cd6c53
    10.1016/j.celrep.2014.10.043
    Scopus Count
    Collections
    All Paterson Institute for Cancer Research

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