MicroRNA Promoter Methylation in Colorectal Cancer

Masoud Asefi, Nayebali Rezvani, Mohammad Hasan Soheilifar, M. Saidijam, Ali Mahdavinezhad
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Abstract

Colorectal cancer (CRC) is one of the most common cancers worldwide. The beginning and progression of the disease are thought to be determined by combinations of epigenetic and genetic changes that trigger multistep programs of carcinogenesis. In colorectal cancer, epigenetic alterations, in particular promoter CpG island methylation, occur more commonly than genetic mutations. Hyper-methylation contributes to carcinogenesis via inducing transcriptional silencing or down-regulation of tumor suppressor genes. DNA methylation alteration has a high potential for minimally invasive biomarker identification. Genome analysis has confirmed that microRNA expression is deregulated in most cancer types through several mechanisms, including failings in the microRNA biogenesis machinery. Moreover, microRNAs can be dysregulated by abnormal CpG methylation in cancer. Since it is believed that epigenetic changes occur in the early stages of the disease, these changes can be used for the early detection of cancer. In this review, we intend to study the role of microRNA gene promoter methylation in colorectal cancer.
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结直肠癌中的MicroRNA启动子甲基化
结直肠癌(CRC)是世界上最常见的癌症之一。这种疾病的开始和发展被认为是由诱发多步骤癌变的表观遗传和遗传变化的组合决定的。在结直肠癌中,表观遗传改变,特别是启动子CpG岛甲基化,比基因突变更常见。超甲基化通过诱导肿瘤抑制基因的转录沉默或下调来促进癌变。DNA甲基化改变在微创生物标志物鉴定中具有很高的潜力。基因组分析证实,在大多数癌症类型中,microRNA的表达是通过几种机制解除调控的,包括microRNA生物发生机制的失败。此外,癌症中CpG甲基化异常会导致microrna失调。由于人们认为表观遗传变化发生在疾病的早期阶段,因此这些变化可用于癌症的早期检测。在这篇综述中,我们打算研究microRNA基因启动子甲基化在结直肠癌中的作用。
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审稿时长
12 weeks
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