在p53缺失的情况下,KLF5通过miR-192靶向ZEB2调控肝癌细胞的上皮-间质转化。

IF 4.3 3区 材料科学 Q1 ENGINEERING, ELECTRICAL & ELECTRONIC
Lan Sun, Xiaona Zhou, Yanmeng Li, Wei Chen, Shanna Wu, Bei Zhang, Jingyi Yao, Anjian Xu
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引用次数: 7

摘要

kr ppel样因子5 (KLF5)可以促进和抑制细胞迁移,但其潜在机制尚未阐明。在本研究中,我们发现KLF5在肝癌细胞上皮-间质转化(EMT)和迁移中的功能取决于细胞肿瘤抗原p53 (p53)的状态。此外,在p53缺失的情况下,锌指e盒结合同源盒2 (ZEB2)是肝癌细胞EMT中KLF5的主要调节因子。最重要的是,p53和KLF5对ZEB2的调控是间接的,miR-192介导了这种调控。最后,我们发现在浸润性肝癌中,在p53缺失或突变的情况下,KLF5缺失。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

KLF5 regulates epithelial-mesenchymal transition of liver cancer cells in the context of p53 loss through miR-192 targeting of ZEB2.

KLF5 regulates epithelial-mesenchymal transition of liver cancer cells in the context of p53 loss through miR-192 targeting of ZEB2.

KLF5 regulates epithelial-mesenchymal transition of liver cancer cells in the context of p53 loss through miR-192 targeting of ZEB2.

KLF5 regulates epithelial-mesenchymal transition of liver cancer cells in the context of p53 loss through miR-192 targeting of ZEB2.

Krüppel-like factor 5 (KLF5) can both promote and suppress cell migration, but the underlying mechanisms have not been elucidated. In this study, we show that the function of KLF5 in epithelial-mesenchymal transition (EMT) and migration of liver cancer cells depends on the status of the cellular tumor antigen p53 (p53). Furthermore, zinc finger E-box-binding homeobox 2 (ZEB2) is the main regulator of KLF5 in EMT in liver cancer cells in the context of p53 loss. Most importantly, the regulation of ZEB2 by p53 and KLF5 is indirect and that miR-192 mediates this regulation. Finally, we find that in invasive liver cancer, KLF5 is absent in the context of p53 loss or mutation.

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CiteScore
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