ILEI: a cytokine essential for EMT, tumor formation, and late events in metastasis in epithelial cells.
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Authors
Waerner, ThomasAlacakaptan, Memetcan
Tamir, Ido
Oberauer, Rupert
Gal, Annamaria
Brabletz, Thomas
Schreiber, Martin
Jechlinger, Martin
Beug, Hartmut
Issue Date
2006-09Subjects
Cellbio
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Show full item recordAbstract
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
ElsevierJournal
Cancer cellPubMed ID
16959614Additional Links
http://www.ncbi.nlm.nih.gov/pubmed/16959614Type
ArticleLanguage
enISSN
1535-6108ae974a485f413a2113503eed53cd6c53
10.1016/j.ccr.2006.07.020