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    ILEI: a cytokine essential for EMT, tumor formation, and late events in metastasis in epithelial cells.

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    Authors
    Waerner, Thomas
    Alacakaptan, Memetcan
    Tamir, Ido
    Oberauer, Rupert
    Gal, Annamaria
    Brabletz, Thomas
    Schreiber, Martin
    Jechlinger, Martin
    Beug, Hartmut
    Issue Date
    2006-09
    Subjects
    Cellbio
    
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    Abstract
    Erk/MAPK and TGFbeta signaling cause epithelial to mesenchymal transition (EMT) and metastasis in mouse mammary epithelial cells (EpH4) transformed with oncogenic Ras (EpRas). In trials to unravel underlying mechanisms, expression profiling for EMT-specific genes identified a secreted interleukin-related protein (ILEI), upregulated exclusively at the translational level. Stable overexpression of ILEI in EpH4 and EpRas cells caused EMT, tumor growth, and metastasis, independent of TGFbeta-R signaling and enhanced by Bcl2. RNAi-mediated knockdown of ILEI in EpRas cells before and after EMT (EpRasXT) prevented and reverted TGFbeta-dependent EMT, also abrogating metastasis formation. ILEI is overexpressed and/or altered in intracellular localization in multiple human tumors, an event strongly correlated to invasion/EMT, metastasis formation, and survival in human colon and breast cancer.
    Citation
    Waerner, T., Alacakaptan, M., Tamir, I., Oberauer, R., Gal, A., Brabletz, T., Schreiber, M., Jechlinger, M., Beug, H. (2006) 'ILEI: a cytokine essential for EMT, tumor formation, and late events in metastasis in epithelial cells', "Cancer Cell", 10(3),pp. 227-239.
    Publisher
    Elsevier
    Journal
    Cancer cell
    URI
    http://hdl.handle.net/10547/294520
    DOI
    10.1016/j.ccr.2006.07.020
    PubMed ID
    16959614
    Additional Links
    http://www.ncbi.nlm.nih.gov/pubmed/16959614
    Type
    Article
    Language
    en
    ISSN
    1535-6108
    ae974a485f413a2113503eed53cd6c53
    10.1016/j.ccr.2006.07.020
    Scopus Count
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    Cell and Cryobiology Research Group

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