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The ubiquitin–proteasome system and signal transduction pathways regulating Epithelial Mesenchymal transition of cancer

机译:泛素 - 蛋白酶体系和信号转导途径调节癌症上皮间充质转换

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Epithelial to Mesenchymal transition (EMT) in cancer, a process permitting cancer cells to become mobile and metastatic, has a signaling hardwire forged from development. Multiple signaling pathways that regulate carcinogenesis enabling characteristics in neoplastic cells such as proliferation, resistance to apoptosis and angiogenesis are also the main players in EMT. These pathways, as almost all cellular processes, are in their turn regulated by ubiquitination and the Ubiquitin-Proteasome System (UPS). Ubiquitination is the covalent link of target proteins with the small protein ubiquitin and serves as a signal to target protein degradation by the proteasome or to other outcomes such as endocytosis, degradation by the lysosome or specification of cellular localization. This paper reviews signal transduction pathways regulating EMT and being regulated by ubiquitination.
机译:上皮对癌症中的间充质转换(EMT),一种允许癌细胞成为移动和转移的过程,具有从发育的信号传导的硬件。调节致癌性能在肿瘤细胞中的多种信号通路,例如增殖,对凋亡和血管生成的耐药性也是EMT中的主要球员。尽管几乎所有细胞过程,这些途径在泛素化和泛素 - 蛋白酶体系(UPS)上调节。泛素是靶蛋白与小蛋白质泛素的共价链接,用作蛋白酶体或其他结果的蛋白质降解的信号,例如内吞作用,通过溶酶体的降解或细胞定位的规格。本文评论了调节EMT的信号转导途径,并通过泛素化调节。

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