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锌指E盒结合蛋白1:处于上皮-间质转化、转移和治疗抗性的交叉点上。

ZEB1: at the crossroads of epithelial-mesenchymal transition, metastasis and therapy resistance.

作者信息

Zhang Peijing, Sun Yutong, Ma Li

机构信息

a Department of Experimental Radiation Oncology.

出版信息

Cell Cycle. 2015;14(4):481-7. doi: 10.1080/15384101.2015.1006048.

Abstract

Zinc finger E-box binding homeobox 1 (ZEB1) is a transcription factor that promotes tumor invasion and metastasis by inducing epithelial-mesenchymal transition (EMT) in carcinoma cells. EMT not only plays an important role in embryonic development and malignant progression, but is also implicated in cancer therapy resistance. It has been hypothesized that carcinoma cells that have undergone EMT acquire cancer stem cell properties including self-renewal, chemoresistance and radioresistance. However, our recent data indicate that ZEB1 regulates radioresistance in breast cancer cells through an EMT-independent mechanism. In this Perspective, we review different mechanisms by which ZEB1 regulates tumor progression and treatment resistance. Based on studies by us and others, we propose that it is specific EMT inducers like ZEB1, but not the epithelial or mesenchymal state itself, that dictate cancer stem cell properties.

摘要

锌指E盒结合同源框1(ZEB1)是一种转录因子,可通过诱导癌细胞的上皮-间质转化(EMT)来促进肿瘤侵袭和转移。EMT不仅在胚胎发育和恶性进展中起重要作用,还与癌症治疗耐药性有关。据推测,经历过EMT的癌细胞会获得癌症干细胞特性,包括自我更新、化学抗性和放射抗性。然而,我们最近的数据表明,ZEB1通过一种不依赖EMT的机制调节乳腺癌细胞的放射抗性。在本观点文章中,我们综述了ZEB1调节肿瘤进展和治疗耐药性的不同机制。基于我们和其他人的研究,我们提出,是像ZEB1这样的特定EMT诱导因子,而非上皮或间质状态本身,决定了癌症干细胞特性。

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