活化的Src通过增强帽依赖性翻译来提高β-连环蛋白的表达。
Active Src elevates the expression of beta-catenin by enhancement of cap-dependent translation.
作者信息
Karni Rotem, Gus Yael, Dor Yuval, Meyuhas Oded, Levitzki Alexander
机构信息
Department of Biological Chemistry, The Alexander Silberman Institute of Life Sciences, The Hebrew University of Jerusalem, 91904 Jerusalem, Israel.
出版信息
Mol Cell Biol. 2005 Jun;25(12):5031-9. doi: 10.1128/MCB.25.12.5031-5039.2005.
Abstract
The proto-oncogene pp60(c-Src) (c-Src) is activated in many types of cancer and contributes to the transformed phenotype of the tumor, although its role is not yet fully understood. Here we report that active Src elevates the levels of beta-catenin by enhancing cap-dependent translation. Src induces phosphorylation of the eukaryotic initiation factor 4E via the Ras/Raf/ERK pathway and the phosphorylation of its inhibitor 4E-BP1 via the PI3K/mTOR pathway. Activated Src enhances the accumulation of nuclear beta-catenin and enhances its transcriptional activity, elevating target genes such as cyclin D1. This novel activation of the Wnt pathway by Src most probably contributes to the oncogenic phenotype of cancer cells.
摘要
原癌基因pp60（c-Src）（c-Src）在多种癌症中被激活，并有助于肿瘤的转化表型，尽管其作用尚未完全明确。在此我们报告，活性Src通过增强帽依赖性翻译提高β-连环蛋白水平。Src通过Ras/Raf/ERK途径诱导真核起始因子4E磷酸化，并通过PI3K/mTOR途径诱导其抑制剂4E-BP1磷酸化。活化的Src增强核β-连环蛋白的积累并增强其转录活性，提高诸如细胞周期蛋白D1等靶基因的表达。Src对Wnt途径的这种新激活很可能促成癌细胞的致癌表型。
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