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首页> 外文期刊>Journal of Cellular Physiology >The ubiquitin ligase TRIM56 inhibits ovarian cancer progression by targeting vimentin
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The ubiquitin ligase TRIM56 inhibits ovarian cancer progression by targeting vimentin

机译：泛素连接酶TRIM56抑制卵巢针对波形蛋白癌症恶化

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摘要

Tumor metastasis is responsible for 90% of all cancer‐related deaths. Epithelial to mesenchymal transition (EMT) is an important prerequisite for tumor metastasis. One of the important mediators of EMT and cancer progression in ovarian cancer is the vimentin protein. The objective of the current study was to evaluate the molecular mechanism that regulates vimentin expression in ovarian cancer cells. Vimentin was robustly induced in the ovarian cancer cell line SKOV‐3 compared to normal ovarian epithelial cell line Moody and the induction was not due to transcriptional upregulation. Treatment with the proteasomal inhibitor MG‐132 revealed that vimentin is actively degraded by the proteasome in Moody cells and stabilized in the SKOV‐3 cell line. Mass spectrometric analysis of vimentin immunoprecipitate of MG‐132 treated Moody cells revealed candidate ubiquitin ligases associated with vimentin. RNAi mediated silencing of the candidate ubiquitin in Moody cells and concurrent overexpression of the candidate ubiquitin ligases in SKOV‐3 confirmed that TRIM56 is the ubiquitin ligase that is degrading vimentin in Moody cells. RNAi mediated silencing of TRIM56 in Moody cells and ectopic overexpression of TRIM56 in SKOV‐3 cells, respectively, significantly up‐ and down‐regulated in vitro migration and invasion in these cells. Analysis of TRIM56 transcript level and vimentin protein expression in 25 patients with ovarian carcinoma confirmed an inverse correlation between TRIM56 and vimentin expression. Cumulatively, our data reveals for the first time a novel post‐translational regulatory mechanism of regulating vimentin expression, EMT, and metastatic progression in ovarian cancer cells.
机译：肿瘤转移90%的负责癌症相关的死亡。过渡(EMT)是一个重要的先决条件肿瘤的转移。卵巢癌的EMT和癌症进展波形蛋白是蛋白质。当前的研究旨在评估分子机制,调节波形蛋白表达卵巢癌细胞。卵巢癌细胞系的诱导SKOV 3相比正常卵巢上皮细胞系喜怒无常,归纳并不是由于转录upregulation。蛋白酶体抑制剂毫克量132显示波形蛋白是积极的蛋白酶体降解在穆迪细胞和稳定SKOV 3细胞线。免疫沉淀反应132毫克量穆迪细胞治疗显示候选人泛素连接酶有关波形蛋白。候选人在穆迪泛素细胞和并发过度的泛素连接酶在SKOV 3确认TRIM56泛素连接酶是降解细胞波形蛋白在喜怒无常。RNAi TRIM56沉默的穆迪细胞介导的和异位的超表达TRIM56 SKOV 3细胞,分别显著》监管的体外迁移和入侵这些细胞。和波形蛋白蛋白表达在25个病人与卵巢癌证实了成反比TRIM56与波形蛋白之间的相关性表达式。小说第一次发布的转化调节波形蛋白的调控机制表情,EMT,转移性进展卵巢癌细胞。

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