YY1在肿瘤发生中的调控及其在肿瘤治疗中的靶向潜力

Guangchao Sui
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引用次数: 37

摘要

阴阳1 (YY1)是一种多功能蛋白,调节多种发育和分化过程。越来越多的证据表明YY1在肿瘤发生中起重要作用。作为一种转录因子,YY1调节了许多主要与癌症有关的基因的表达。YY1可以激活或抑制目标基因,这取决于它招募的辅助因子。重要的是,迄今为止的大多数研究表明,YY1在癌症发展中具有增生性或致癌作用。同时,YY1在不同类型的癌症中均有过表达,并被认为是这些癌症的潜在预后标志物。一个合理的假设是,YY1的上调导致其靶基因的不平衡表达,进而引发或争论肿瘤的发生。大量研究表明,YY1在多种表观遗传事件中发挥着广泛的调控作用,尤其是组蛋白乙酰化和甲基化。由于大多数癌症表现出不受调控的表观遗传学,YY1的过度表达可能导致癌细胞中这些异常的表观遗传学状态。由YY1调控的表观遗传过程是可逆的。因此,靶向YY1可能会调节癌细胞中各种失调的表观遗传事件,恢复正常的表观遗传状况,从而阻断癌症的发展。本文综述了YY1的肿瘤相关研究,并讨论了YY1作为肿瘤治疗靶点的潜力。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
The Regulation of YY1 in Tumorigenesis and its Targeting Potential in Cancer Therapy
Yin Yang 1 (YY1) is a multifunctional protein and regulates various processes of development and differentiation. Increasing evidence indicates an essential role of YY1 in tumorigenesis. As a transcription factor, YY1 regulates the expression of numerous genes that are mostly involved in cancers. YY1 can either activate or repress the target genes, depending on the cofactors that it recruits. Importantly, most studies to date suggest a proliferative or oncogenic role of YY1 in cancer development. Meanwhile, overexpression of YY1 has been observed in different types of cancers and YY1 has been proposed as a potential prognostic marker of these cancers. A reasonable hypothesis is that upregulated YY1 leads to unbalanced expression of its target genes and in turn initiates or arguments tumorigenesis. Ample studies indicate that YY1 exerts broad regulation in various epigenetic events, especially histone acetylation and methylation. Since most cancers exhibit deregulated epigenetics, overexpressed YY1 may contribute to these aberrant epigenetic statuses in cancer cells. The epigenetic processes regulated by YY1 are reversible. Therefore, it is possible that targeting YY1 may adjust various deregulated epigenetic events in cancer cells, restore the normal epigenetic conditions and consequently block cancer development. This review summarizes cancer-related studies of YY1 and discusses the potential of YY1 as a target of cancer therapy.
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