Expression of a translationally regulated, dominant-negative CCAAT/enhancer-binding protein beta isoform and up-regulation of the eukaryotic translation initiation factor 2alpha are correlated with neoplastic transformation of mammary epithelial cells.
Expression of a translationally regulated, dominant-negative CCAAT/enhancer-binding protein beta isoform and up-regulation of the eukaryotic translation initiation factor 2alpha are correlated with neoplastic transformation of mammary epithelial cells.
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发表时间：
1996-10
期刊：
影响因子：
11.2
通讯作者：
B. Raught;A. Gingras;A. James;D. Medina;N. Sonenberg;J. Rosen
中科院分区：
文献类型：
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作者：
B. Raught;A. Gingras;A. James;D. Medina;N. Sonenberg;J. Rosen
CCAAT/增强子结合蛋白β的翻译调节、显性失活亚型在不同病因的可移植性和原发性小鼠乳腺肿瘤中表达，但在肿瘤前乳腺增生或原发性前列腺、肺、晶状体、卵巢或淋巴肿瘤中不表达。与正常组织和增生组织相比，真核起始因子 2α 蛋白在这些乳腺肿瘤中的表达水平也显着升高 (69.8 +/- 7.2%)。因此，真核起始因子2α的错误调节可能促进显性失活CCAAT/增强子结合蛋白β亚型的表达，这可能抑制终末分化并促进乳腺上皮细胞不受控制的增殖。
A translationally regulated, dominant-negative isoform of CCAAT/enhancer-binding protein beta is expressed in transplantable and primary mouse mammary tumors of different etiologies but is not expressed in preneoplastic mammary hyperplasias or in primary prostate, lung, lens, ovary or lymphoid tumors. The eukaryotic initiation factor 2alpha protein is also expressed at significantly higher levels (69.8 +/- 7.2%) in these mammary tumors compared with normal and hyperplastic tissues. Thus, misregulation of eukaryotic initiation factor 2alpha may promote the expression of a dominant-negative CCAAT/enhancer-binding protein beta isoform, which may inhibit terminal differentiation and facilitate uncontrolled proliferation of mammary epithelial cells.