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本文引用的文献

1
Cyclin-dependent kinase 1 (CDK1)-mediated phosphorylation of enhancer of zeste 2 (Ezh2) regulates its stability.周期素依赖性激酶 1(CDK1)介导的增强子结合蛋白 2(Ezh2)的磷酸化调节其稳定性。
J Biol Chem. 2011 Aug 12;286(32):28511-9. doi: 10.1074/jbc.M111.240515. Epub 2011 Jun 9.
2
Pharmacologic disruption of Polycomb Repressive Complex 2 inhibits tumorigenicity and tumor progression in prostate cancer.药物破坏 Polycomb 抑制复合物 2 可抑制前列腺癌的致瘤性和肿瘤进展。
Mol Cancer. 2011 Apr 18;10:40. doi: 10.1186/1476-4598-10-40.
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Aberrations of EZH2 in cancer.EZH2 基因在癌症中的异常。
Clin Cancer Res. 2011 May 1;17(9):2613-8. doi: 10.1158/1078-0432.CCR-10-2156. Epub 2011 Mar 2.
4
Ovarian cancer stem cell-like side populations are enriched following chemotherapy and overexpress EZH2.卵巢癌细胞样侧群细胞在化疗后富集,并过度表达 EZH2。
Mol Cancer Ther. 2011 Feb;10(2):325-35. doi: 10.1158/1535-7163.MCT-10-0788. Epub 2011 Jan 7.
5
EZH2 promotes expansion of breast tumor initiating cells through activation of RAF1-β-catenin signaling.EZH2 通过激活 RAF1-β-连环蛋白信号促进乳腺肿瘤起始细胞的扩增。
Cancer Cell. 2011 Jan 18;19(1):86-100. doi: 10.1016/j.ccr.2010.10.035. Epub 2011 Jan 6.
6
Epigenetic factors in cancer development: polycomb group proteins.癌症发生发展中的表观遗传因素:多梳蛋白家族。
Future Oncol. 2011 Jan;7(1):57-75. doi: 10.2217/fon.10.157.
7
CDK1-dependent phosphorylation of EZH2 suppresses methylation of H3K27 and promotes osteogenic differentiation of human mesenchymal stem cells.CDK1 依赖性磷酸化 EZH2 抑制 H3K27 的甲基化,促进人骨髓间充质干细胞的成骨分化。
Nat Cell Biol. 2011 Jan;13(1):87-94. doi: 10.1038/ncb2139. Epub 2010 Dec 5.
8
Phosphorylation of the PRC2 component Ezh2 is cell cycle-regulated and up-regulates its binding to ncRNA.PRC2 组件 Ezh2 的磷酸化受细胞周期调控,并上调其与 ncRNA 的结合。
Genes Dev. 2010 Dec 1;24(23):2615-20. doi: 10.1101/gad.1983810.
9
Epigenetic antagonism between polycomb and SWI/SNF complexes during oncogenic transformation.抑癌基因与癌基因的表达调控
Cancer Cell. 2010 Oct 19;18(4):316-28. doi: 10.1016/j.ccr.2010.09.006.
10
Cyclin-dependent kinases regulate epigenetic gene silencing through phosphorylation of EZH2.细胞周期蛋白依赖性激酶通过磷酸化 EZH2 调节表观遗传基因沉默。
Nat Cell Biol. 2010 Nov;12(11):1108-14. doi: 10.1038/ncb2116. Epub 2010 Oct 10.

EZH2 在肿瘤进展中的作用。

The role of EZH2 in tumour progression.

机构信息

Department of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.

出版信息

Br J Cancer. 2012 Jan 17;106(2):243-7. doi: 10.1038/bjc.2011.551. Epub 2011 Dec 20.

DOI:10.1038/bjc.2011.551
PMID:22187039
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3261672/
Abstract

Accumulated evidence shows that EZH2 is deregulated in a wide range of cancer types, and it has a crucial role in stem cell maintenance and tumour development. Therefore, blocking EZH2 expression or activity may represent a promising strategy for anticancer treatment. In this review, we address the current understanding of the mechanisms underlying EZH2 regulation alongside the function of EZH2 gene targets that are involved in cancer progression. Finally, we will describe cancer therapies that target EZH2 or its downstream cascades, which could potentially reverse the oncogenic and stemness properties of the tumour cells to suppress cancer progression and recurrence.

摘要

积累的证据表明,EZH2 在广泛的癌症类型中失调,并且在干细胞维持和肿瘤发展中起着关键作用。因此,阻断 EZH2 的表达或活性可能代表着一种有前途的抗癌治疗策略。在这篇综述中,我们讨论了 EZH2 调节的机制以及 EZH2 基因靶点在癌症进展中的功能的最新认识。最后,我们将描述针对 EZH2 或其下游级联的癌症治疗方法,这些方法可能逆转肿瘤细胞的致癌和干性特性,从而抑制癌症的进展和复发。