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TET1 regulates hypoxia-induced epithelial-mesenchymal transition by acting as a co-activator

机译:TET1通过充当共激活因子调节缺氧诱导的上皮-间质转化

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摘要

Background: Hypoxia induces the epithelial-mesenchymal transition, EMT, to promote cancer metastasis. In addition to transcriptional regulation mediated by hypoxia-inducible factors, HIFs, other epigenetic mechanisms of gene regulation, such as histone modifications and DNA methylation, are utilized under hypoxia. However, whether DNA demethylation mediated by TET1, a DNA dioxygenase converting 5-methylcytosine, 5mC, into 5-hydroxymethylcytosine, 5hmC, plays a role in hypoxia-induced EMT is largely unknown.
机译:背景:低氧诱导上皮-间质转化,EMT,以促进癌症转移。除缺氧诱导因子介导的转录调控外,在缺氧条件下还利用了HIF,基因调控的其他表观遗传机制,如组蛋白修饰和DNA甲基化。然而,由TET1介导的将5mC的5-甲基胞嘧啶转化为5hmC的5-羟甲基胞嘧啶的DNA双加氧酶介导的DNA脱甲基作用是否在缺氧诱导的EMT中发挥作用尚不清楚。

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