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首页> 外文期刊>Journal of Cellular Physiology >Loss of TET1 facilitates DLD1 colon cancer cell migration via H3K27me3‐mediated down‐regulation of E‐cadherin
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Loss of TET1 facilitates DLD1 colon cancer cell migration via H3K27me3‐mediated down‐regulation of E‐cadherin

机译：TET1促进DLD1结肠癌细胞的损失移民通过H3K27me3介导下应承担的监管

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摘要

Epigenetic modifications such as histone modifications and cytosine hydroxymethylation are linked to tumorigenesis. Loss of 5‐hydroxymethylcytosine (5?hmC) by ten‐eleven translocation 1 (TET1) down‐regulation facilitates tumor initiation and development. However, the mechanisms by which loss of TET1 knockdown promotes malignancy development remains unclear. Here, we report that TET1 knockdown induced epithelial‐mesenchymal transition (EMT) and increased cancer cell growth, migration, and invasion in DLD1 cells. Loss of TET1 increased EZH2 expression and reduced UTX‐1 expression, thus increasing histone H3K27 tri‐methylation causing repression of the target gene E‐cadherin. Ectopic expression of the H3K27 demethylase UTX‐1 or EZH2 depletion both impeded EZH2 binding caused a loss of H3K27 methylation at epithelial gene E‐cadherin promoter, thereby suppressing EMT and tumor invasion in shTET1 cells. Conversely, UTX‐1 depletion and ectopic expression of EZH2 enhanced EMT and tumor metastasis in DLD1 cells. These findings provide insight into the regulation of TET1 and E‐cadherin and identify EZH2 as a critical mediator of E‐cadherin repression and tumor progression.
机译：表观遗传修饰,如组蛋白修改和胞嘧啶hydroxymethylation与肿瘤发生有关。5必经hydroxymethylcytosine (5 ? hmC), 10的11易位1 (TET1)下的监管促进肿瘤发生和发展。然而,TET1损失的机制可拆卸的促进恶性肿瘤发展仍然存在不清楚。诱导上皮间充质转变(EMT)应承担的和增加癌症细胞生长、迁移和在细胞DLD1入侵。EZH2表达式和减少属下1表达,从而增加组蛋白H3K27三甲基化导致目标基因的镇压E钙粘素。异位表达的H3K27 demethylase属下1或EZH2损耗都阻碍EZH2绑定造成的损失在上皮H3K27甲基化高钙粘着蛋白启动子区域基因E,从而抑制EMT在shTET1细胞和肿瘤入侵。属下1 EZH2的耗竭和异位表达增强EMT在DLD1细胞和肿瘤转移。这些发现提供了深入的了解监管TET1和E钙粘素和识别EZH2的关键中介E钙粘素镇压和肿瘤进展。

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