Regulation of EMT in Colorectal Cancer: A Culprit in Metastasis.
Regulation of EMT in Colorectal Cancer: A Culprit in Metastasis.
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DOI：
10.3390/cancers9120171
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发表时间：
2017-12-16
期刊：
影响因子：
5.2
通讯作者：
Datta PK
中科院分区：
文献类型：
--
作者：
Vu T;Datta PK
上皮向间质转化（EMT）是细胞失去其上皮特性（例如细胞极性和细胞-细胞接触）并获得间质特性（例如运动性增加）的过程。在结直肠癌（CRC）中，EMT与侵袭性或转移性表型相关。在这篇综述中，我们讨论了最近的研究探索新的调控机制，EMT在CRC，包括新的CRC EMT调节剂的识别。诱导物的上调可促进EMT，导致CRC中侵袭和转移增加。这些诱导剂可以通过调节EMT相关信号传导途径（例如WNT/β-连环蛋白和TGF-β）和EMT转录因子（例如锌指E盒结合同源框1（ZEB 1）和ZEB 2）来下调E-钙粘蛋白并上调N-钙粘蛋白和波形蛋白（Vim）。此外，发现包括miR-34和miR-200家族成员在内的几种microRNA（miRNA）靶向EMT转录因子的mRNA，例如ZEB 1、ZEB 2或SNAIL。这些miRNA的下调与远处转移和晚期肿瘤相关。此外，EMT在循环肿瘤细胞（CTC）中的作用也进行了讨论。发现EMT CTC表面上的间充质标志物与转移相关，并且可以作为转移的潜在生物标志物。总之，这些研究表明，EMT是由一个复杂的网络精心策划的，涉及不同信号通路的调节器。需要进一步的研究来了解CRC中EMT的潜在机制。
Epithelial to mesenchymal transition (EMT) is a process during which cells lose their epithelial characteristics, for instance cell polarity and cell–cell contact, and gain mesenchymal properties, such as increased motility. In colorectal cancer (CRC), EMT is associated with an invasive or metastatic phenotype. In this review, we discuss recent studies exploring novel regulation mechanisms of EMT in CRC, including the identification of new CRC EMT regulators. Upregulation of inducers can promote EMT, leading to increased invasiveness and metastasis in CRC. These inducers can downregulate E-cadherin and upregulate N-cadherin and vimentin (VIM) through modulating EMT-related signaling pathways, for instance WNT/β-catenin and TGF-β, and EMT transcription factors, such as zinc finger E-box binding homeobox 1 (ZEB1) and ZEB2. In addition, several microRNAs (miRNAs), including members of the miR-34 and miR-200 families, are found to target mRNAs of EMT-transcription factors, for example ZEB1, ZEB2, or SNAIL. Downregulation of these miRNAs is associated with distant metastasis and advanced stage tumors. Furthermore, the role of EMT in circulating tumor cells (CTCs) is also discussed. Mesenchymal markers on the surface of EMT CTCs were found to be associated with metastasis and could serve as potential biomarkers for metastasis. Altogether, these studies indicate that EMT is orchestrated by a complicated network, involving regulators of different signaling pathways. Further studies are required to understand the mechanisms underlying EMT in CRC.
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作者：
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