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首页> 外文期刊>Cancer Cell >PKD1 phosphorylation-dependent degradation of SNAIL by SCF-FBXO11 regulates epithelial-mesenchymal transition and metastasis.
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PKD1 phosphorylation-dependent degradation of SNAIL by SCF-FBXO11 regulates epithelial-mesenchymal transition and metastasis.

机译：SCF-FBXO11对SNAIL的PKD1磷酸化依赖性降解可调节上皮-间质转化和转移。

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摘要

Metastatic dissemination is often initiated by the reactivation of an embryonic development program referred to as epithelial-mesenchymal transition (EMT). The transcription factor SNAIL promotes EMT and elicits associated pathological characteristics such as invasion, metastasis, and stemness. To better understand the posttranslational regulation of SNAIL, we performed a luciferase-based, genome-wide E3 ligase siRNA library screen and identified SCF-FBXO11 as an important E3 that targets SNAIL for ubiquitylation and degradation. Furthermore, we discovered that SNAIL degradation by FBXO11 is dependent on Ser-11 phosphorylation of SNAIL by protein kinase D1 (PKD1). FBXO11 blocks SNAIL-induced EMT, tumor initiation, and metastasis in multiple breast cancer models. These findings establish the PKD1-FBXO11-SNAIL axis as a mechanism of posttranslational regulation of EMT and cancer metastasis.
机译：转移性传播通常是通过重新激活称为上皮-间质转化（EMT）的胚胎发育程序而开始的。转录因子SNAIL促进EMT并引起相关的病理学特征，例如侵袭，转移和干性。为了更好地理解SNAIL的翻译后调控，我们进行了基于荧光素酶的全基因组E3连接酶siRNA文库筛选，并将SCF-FBXO11确定为靶向SNAIL的泛素化和降解的重要E3。此外，我们发现FBXO11对SNAIL的降解取决于蛋白激酶D1（PKD1）对SNAIL的Ser-11磷酸化作用。 FBXO11可在多种乳腺癌模型中阻断SNAIL诱导的EMT，肿瘤起始和转移。这些发现将PKD1-FBXO11-SNAIL轴确立为EMT和癌症转移的翻译后调控机制。

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