ILEI：一种上皮细胞中EMT、肿瘤形成及转移后期事件所必需的细胞因子。
ILEI: a cytokine essential for EMT, tumor formation, and late events in metastasis in epithelial cells.
作者信息
Waerner Thomas, Alacakaptan Memetcan, Tamir Ido, Oberauer Rupert, Gal Annamaria, Brabletz Thomas, Schreiber Martin, Jechlinger Martin, Beug Hartmut
机构信息
Research Institute of Molecular Pathology, Dr. Bohrgasse 7, A-1030 Vienna, Austria.
出版信息
Cancer Cell. 2006 Sep;10(3):227-39. doi: 10.1016/j.ccr.2006.07.020.
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.
Erk/MAPK和TGFβ信号通路可导致用致癌Ras（EpRas）转化的小鼠乳腺上皮细胞（EpH4）发生上皮-间质转化（EMT）和转移。在探究潜在机制的试验中，对EMT特异性基因进行表达谱分析，鉴定出一种分泌的白细胞介素相关蛋白（ILEI），其仅在翻译水平上调。ILEI在EpH4和EpRas细胞中的稳定过表达导致EMT、肿瘤生长和转移，与TGFβ-R信号通路无关，并被Bcl2增强。在EMT前后（EpRasXT），RNAi介导的EpRas细胞中ILEI的敲低可预防和逆转TGFβ依赖性EMT，也可消除转移形成。ILEI在多种人类肿瘤中过表达和/或细胞内定位改变，这一事件与人类结肠癌和乳腺癌的侵袭/EMT、转移形成及生存密切相关。
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