ILEI: a cytokine essential for EMT, tumor formation, and late events in metastasis in epithelial cells
Autor: | Rupert Oberauer, Martin Schreiber, Martin Jechlinger, Hartmut Beug, Annamaria Gal, Thomas Brabletz, Memetcan Alacakaptan, Thomas Waerner, Ido Tamir |
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Rok vydání: | 2005 |
Předmět: |
MAPK/ERK pathway
Cancer Research Time Factors medicine.medical_treatment Cellular differentiation Metastasis Cell Line Mice Downregulation and upregulation Transforming Growth Factor beta Neoplasms medicine Animals Humans Epithelial–mesenchymal transition RNA Messenger Neoplasm Metastasis Mice Inbred BALB C biology Cell Differentiation Epithelial Cells Mesenchymal Stem Cells Cell Biology Transforming growth factor beta medicine.disease Prognosis Neoplasm Proteins Gene Expression Regulation Neoplastic Survival Rate Cytokine Cell Transformation Neoplastic Oncology Protein Biosynthesis embryonic structures Immunology biology.protein Cancer research Cytokines CELLBIO RNA Interference Signal transduction Neoplasm Transplantation Signal Transduction |
Zdroj: | University of Brighton |
ISSN: | 1535-6108 |
Popis: | 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. |
Databáze: | OpenAIRE |
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