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[求助]
DNA methylation-associated silencing of tumor-suppressor microRNAs in cancer
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幾句翻譯不出來的 1 Considering the genomic rearrangements, copy-number alterations and translocations that many cancer cells suffer and that give rise to altered levels of the transcripts, changes in the tumoral cell phenotype can be due not only to the protein alteration itself, but also to global RNA deregulation by altered competition for miRNAs 2 This mechanism creates a feedback relationship taking into account that miR-103/107 are both generated by and regulators of Dicer, producing a downscaling of Dicer levels but not their complete depletion, maintaining a basal level to regulate the miRNA pathway. 3 iRNAs transcribed from CpG islands undergo DNA methylation-associated repression with a similar chromatin context to coding genes, such as binding of the transcriptional repressor methyl-CpG-binding domain proteins (Lujambio et al., 2007; Urdinguio et al., 2010), and a histone modification profile associated with silencing, such as in the case of loss of acetylation of histones H3 and H4 (Lujambio et al., 2007; Toyota et al., 2008). |
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呵呵,隔行如隔山,由于不是這個(gè)專業(yè)的,所以翻譯起來很累,而且不一定譯得對,F(xiàn)在提供譯文如下,希望大家批評指正。多謝! 1. 鑒于基因重組、拷貝數(shù)量變化以及導(dǎo)致許多癌細(xì)胞經(jīng)歷并引起轉(zhuǎn)錄水平改變的易位,腫瘤細(xì)胞顯型的變化不僅是蛋白質(zhì)自身變化導(dǎo)致的,也是競爭miRNAs的變化造成了全RNA反常所致。 2. 該機(jī)理產(chǎn)生一種反饋關(guān)系,這種關(guān)系重視miR-103/107的形成和Dicer基因的調(diào)控因子,引起Dicer基因水平的下降但尚未完全損耗,而是維持在能夠調(diào)控miRNA路徑的基礎(chǔ)水平。 3. 由于相似染色體的作用,由CpG島轉(zhuǎn)錄形成的iRNAs受到了與DNA甲基化有關(guān)的抑制作用。該染色體與編碼基因和組蛋白變性有關(guān),前者如結(jié)合轉(zhuǎn)錄抑制因子甲基-CpG-結(jié)合區(qū)域蛋白質(zhì)(盧哈姆比奧等,2007;沃丁谷伊奧等,2010),后者與基因靜默有關(guān),如組蛋白H3和H4的乙;饔貌蛔氵@種情況。 |


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