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微小RNA-204/锌指E盒结合蛋白2轴在乳腺癌中作为转移相关肺腺癌转录本1诱导的上皮-间质转化的关键介质发挥作用。

MiR-204/ZEB2 axis functions as key mediator for MALAT1-induced epithelial-mesenchymal transition in breast cancer.

作者信息

Wang Yuzhou, Zhou Yijin, Yang Zhicheng, Chen Baoying, Huang Wennan, Liu Yongyuan, Zhang Ying

机构信息

Oncology Center, Affiliated Hospital of Guangdong Medical College, Zhanjiang, China.

出版信息

Tumour Biol. 2017 Jul;39(7):1010428317690998. doi: 10.1177/1010428317690998.

DOI:10.1177/1010428317690998
PMID:28675122
Abstract

Long non-coding RNAs recently were identified as key mediators of cancer metastasis. This study provided evidence that long non-coding RNA MALAT1 was up-regulated in breast cancer tissues and cell lines. MALAT1 promoted cancer cell invasion through inducing epithelial-mesenchymal transition. Interestingly, we revealed there was a reciprocal repression between MALAT1 and miR-204. ZEB2 was identified as a downstream target of miR-204 and MALAT1 exerted its function mainly through the miR-204/ZEB2 axis. Our findings suggested that MALAT1 may serve as a new diagnostic biomarker and therapy target for breast cancer.

摘要

长链非编码RNA最近被确定为癌症转移的关键介质。这项研究提供了证据,表明长链非编码RNA MALAT1在乳腺癌组织和细胞系中上调。MALAT1通过诱导上皮-间质转化促进癌细胞侵袭。有趣的是,我们发现MALAT1和miR-204之间存在相互抑制作用。ZEB2被确定为miR-204的下游靶点,MALAT1主要通过miR-204/ZEB2轴发挥其功能。我们的研究结果表明,MALAT1可能作为乳腺癌的一种新的诊断生物标志物和治疗靶点。

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MiR-204/ZEB2 axis functions as key mediator for MALAT1-induced epithelial-mesenchymal transition in breast cancer.微小RNA-204/锌指E盒结合蛋白2轴在乳腺癌中作为转移相关肺腺癌转录本1诱导的上皮-间质转化的关键介质发挥作用。
Tumour Biol. 2017 Jul;39(7):1010428317690998. doi: 10.1177/1010428317690998.
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