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DNA methylation-associated silencing of tumor-suppressor microRNAs in cancer
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几句翻译不出来的 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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爱与雨下(金币+1): !~ 2011-09-23 08:46:22
sltmac(金币+10, 翻译EPI+1): 2011-09-26 07:02:15
sltmac: 辛苦,欢迎常来 2011-09-26 07:02:21
爱与雨下(金币+1): !~ 2011-09-23 08:46:22
sltmac(金币+10, 翻译EPI+1): 2011-09-26 07:02:15
sltmac: 辛苦,欢迎常来 2011-09-26 07:02:21
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呵呵,隔行如隔山,由于不是这个专业的,所以翻译起来很累,而且不一定译得对。现在提供译文如下,希望大家批评指正。多谢! 1. 鉴于基因重组、拷贝数量变化以及导致许多癌细胞经历并引起转录水平改变的易位,肿瘤细胞显型的变化不仅是蛋白质自身变化导致的,也是竞争miRNAs的变化造成了全RNA反常所致。 2. 该机理产生一种反馈关系,这种关系重视miR-103/107的形成和Dicer基因的调控因子,引起Dicer基因水平的下降但尚未完全损耗,而是维持在能够调控miRNA路径的基础水平。 3. 由于相似染色体的作用,由CpG岛转录形成的iRNAs受到了与DNA甲基化有关的抑制作用。该染色体与编码基因和组蛋白变性有关,前者如结合转录抑制因子甲基-CpG-结合区域蛋白质(卢哈姆比奥等,2007;沃丁谷伊奥等,2010),后者与基因静默有关,如组蛋白H3和H4的乙酰化作用不足这种情况。 |

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