DNA Methylation in Cancer Tissues

Daud Faran Asif, M. Naveed, U. Rashid
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引用次数: 2

Abstract

Cancer linked DNA hypo-methylation and hyper-methylation are present throughout the human genome. The hyper-methylation facilitates cancer progress by repressing the tumor suppressor gene. Hypo-methylation contribution towards cancer has not yet been clear. Recent studies of tissue specific methylation have suggested that DNA hypo-methylation aid tumor formation by many pathways. Loss of DNA methylation associated with cancer may alter transcription. In addition, DNA hypo-methylation might affect promoter usage production of intra-genic non-coding RNA transcripts, co-transcriptional splicing and initiation and elongation of transcription. Studies of hemi methylation of DNA in cancerous cells as well as normal tissues suggest that active de-methylation can explain cancer associated DNA hypo-methylation. New studies that genomic 5-hydroxymethylcytosine is intermediate in DNA de-methylation exhibits cancer associated losses. It suggests that both decreased hydroxyl-methylation and methylation of DNA play important role in carcinogenesis.
癌症组织中的DNA甲基化
与癌症相关的DNA低甲基化和高甲基化存在于整个人类基因组中。超甲基化通过抑制肿瘤抑制基因促进癌症进展。低甲基化对癌症的影响尚不清楚。最近对组织特异性甲基化的研究表明,DNA低甲基化通过多种途径帮助肿瘤的形成。与癌症相关的DNA甲基化缺失可能会改变转录。此外,DNA低甲基化可能影响启动子的使用、基因内非编码RNA转录物的产生、共转录剪接以及转录的起始和延伸。对癌细胞和正常组织中DNA半甲基化的研究表明,活跃的去甲基化可以解释癌症相关的DNA低甲基化。新的研究表明,基因组5-羟甲基胞嘧啶是DNA去甲基化的中间产物,显示出癌症相关的损失。提示羟基甲基化和DNA甲基化的降低在癌变过程中起重要作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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