Implications of miR cluster 143/145 as universal anti-oncomiRs and their dysregulation during tumorigenesis.

Implications of miR cluster 143/145 as universal anti-oncomiRs and their dysregulation during tumorigenesis.
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DOI:
10.1186/s12935-015-0247-4
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发表时间:
2015
影响因子:
5.8
通讯作者:
Pillai RM
Pillai RM
中科院分区:
医学2区
文献类型:
--
作者:
Das AV;Pillai RM

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肿瘤发生是一个多步骤的过程,由于癌基因和抗癌基因的不平衡而失调,导致组织稳态破坏。在许多情况下,癌基因和抗癌基因的作用是由各种其他分子(例如 microRNA)介导的。 microRNA 是一种小型非编码 RNA,用于转录后调节一半以上的蛋白质编码基因。 miR簇143/145就是这样一种与癌症相关的microRNA簇,它在大多数癌症中下调,并且能够通过靶向肿瘤相关基因来阻碍肿瘤发生。事实上,它们可以通过靶向多重耐药基因来使耐药癌细胞变得敏感,这使得它们成为靶向癌细胞的有效工具。它们的低水平先于导致癌症进展的事件,因此也可以被视为疾病分期的生物标志物。有趣的是,有证据表明存在几种体内机制,通过这些机制,该簇在分子水平上受到差异性调节,以保持其在癌症中的低水平。在这篇综述中,我们总结了 miR 簇 143/145 在癌症中的作用、它们潜在的预后应用以及它们在肿瘤发生过程中的调节。
Tumorigenesis is a multistep process, de-regulated due to the imbalance of oncogenes as well as anti-oncogenes, resulting in disruption of tissue homeostasis. In many cases the effect of oncogenes and anti-oncogenes are mediated by various other molecules such as microRNAs. microRNAs are small non-coding RNAs established to post-transcriptionally regulate more than half of the protein coding genes. miR cluster 143/145 is one such cancer-related microRNA cluster which is down-regulated in most of the cancers and is able to hinder tumorigenesis by targeting tumor-associated genes. The fact that they could sensitize drug-resistant cancer cells by targeting multidrug resistant genes makes them potent tools to target cancer cells. Their low levels precede events which lead to cancer progression and therefore could be considered also as biomarkers to stage the disease. Interestingly, evidence suggests the existence of several in vivo mechanisms by which this cluster is differentially regulated at the molecular level to keep their levels low in cancer. In this review, we summarize the roles of miR cluster 143/145 in cancer, their potential prognostic applications and also their regulation during tumorigenesis.
DOI: 10.1371/journal.pone.0098140
发表时间: 2014
期刊: PloS one
影响因子: 3.7
作者:
Zhu L;Liu J;Liang F;Rayner S;Xiong J
通讯作者: Xiong J