• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

癌症发生发展中的表观遗传因素:多梳蛋白家族。

Epigenetic factors in cancer development: polycomb group proteins.

机构信息

Department of Experimental Oncology, European Institute of Oncology, IFOM-IEO Campus, Via Adamello 16, Milan, Italy.

出版信息

Future Oncol. 2011 Jan;7(1):57-75. doi: 10.2217/fon.10.157.

DOI:10.2217/fon.10.157
PMID:21174538
Abstract

The role of chromatin-modifying factors in cancer biology emerged exponentially in the last 10 years, and increased attention has been focused on Polycomb group (PcG) proteins and their enzymatic activities. PcG proteins are repressive chromatin modifiers required for proliferation and development. The frequent deregulation of PcG activities in human tumors has direct oncogenic effects and results, essential for cancer cell proliferation. Here we will review the recent findings regarding PcG proteins in prospective tumor development, focusing on the molecular mechanisms that deregulate PcG expression in different tumors, at the downstream pathways to PcG expression (that contribute to cancer development) and at the mechanisms that regulate PcG recruitment to specific targets. Finally, we will speculate on the benefit of PcG inhibition for cancer treatment, reviewing potential pharmacological strategies.

摘要

在过去的 10 年中,染色质修饰因子在癌症生物学中的作用呈指数级增长,人们越来越关注 Polycomb 组(PcG)蛋白及其酶活性。PcG 蛋白是增殖和发育所必需的抑制性染色质修饰因子。PcG 活性在人类肿瘤中的频繁失调具有直接的致癌作用,并对癌细胞的增殖至关重要。在这里,我们将回顾最近关于 PcG 蛋白在肿瘤发生中的作用的发现,重点讨论不同肿瘤中 PcG 表达失调的分子机制,以及 PcG 表达下游途径(有助于癌症发生)和调节 PcG 蛋白募集到特定靶点的机制。最后,我们将推测 PcG 抑制对癌症治疗的益处,回顾潜在的药物治疗策略。

相似文献

1
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.
2
Gene silencing by the Polycomb group proteins and associations with cancer.多梳蛋白组基因沉默与癌症的关联。
Cancer Invest. 2011 Mar;29(3):187-95. doi: 10.3109/07357907.2010.512605. Epub 2011 Feb 4.
3
Epigenetic regulators: Polycomb-miRNA circuits in cancer.表观遗传调控因子:癌症中的多梳蛋白-微小RNA信号通路
Biochim Biophys Acta. 2016 May;1859(5):697-704. doi: 10.1016/j.bbagrm.2016.03.005. Epub 2016 Mar 11.
4
Recruitment of polycomb group complexes and their role in the dynamic regulation of cell fate choice.多梳蛋白复合体的募集及其在细胞命运选择动态调控中的作用。
Development. 2009 Nov;136(21):3531-42. doi: 10.1242/dev.033902.
5
Concise review: roles of polycomb group proteins in development and disease: a stem cell perspective.简要综述:多梳蛋白家族在发育和疾病中的作用:干细胞视角
Stem Cells. 2007 Oct;25(10):2498-510. doi: 10.1634/stemcells.2006-0608. Epub 2007 Jun 28.
6
PRC1 marks the difference in plant PcG repression.PRC1 标志着植物 PcG 抑制作用的差异。
Mol Plant. 2014 Mar;7(3):459-71. doi: 10.1093/mp/sst150. Epub 2013 Oct 31.
7
The emerging role of Polycomb repressors in the response to DNA damage.多梳抑制复合物在 DNA 损伤应答中的新兴作用。
J Cell Sci. 2012 Sep 1;125(Pt 17):3939-48. doi: 10.1242/jcs.107375.
8
Deregulated expression of Polycomb-group oncogenes in human malignant lymphomas and epithelial tumors.多梳蛋白家族癌基因在人类恶性淋巴瘤和上皮性肿瘤中的表达失调。
Hum Mol Genet. 2005 Apr 15;14 Spec No 1:R93-R100. doi: 10.1093/hmg/ddi111.
9
Programming of gene expression by Polycomb group proteins.多梳蛋白家族对基因表达的编程调控
Trends Cell Biol. 2008 May;18(5):236-43. doi: 10.1016/j.tcb.2008.02.005. Epub 2008 Mar 28.
10
Polycomb Group (PcG) Proteins and Human Cancers: Multifaceted Functions and Therapeutic Implications.多梳蛋白家族(PcG)与人类癌症:多方面功能及治疗意义
Med Res Rev. 2015 Nov;35(6):1220-67. doi: 10.1002/med.21358. Epub 2015 Jul 30.

引用本文的文献

1
The first embryo, the origin of cancer and animal phylogeny. V. Cancer stem cells as the unifying biomechanical principle between embryology and oncology.首个胚胎、癌症起源与动物系统发育。五、癌症干细胞作为胚胎学与肿瘤学之间统一的生物力学原理。
Mechanobiol Med. 2024 Dec 5;3(1):100110. doi: 10.1016/j.mbm.2024.100110. eCollection 2025 Mar.
2
EZH2 Contributes to Anoikis Resistance and Promotes Epithelial Ovarian Cancer Peritoneal Metastasis by Regulating m6A.EZH2 通过调控 m6A 促进上皮性卵巢癌腹膜转移并赋予其抗凋亡能力
Curr Med Sci. 2023 Aug;43(4):794-802. doi: 10.1007/s11596-023-2719-4. Epub 2023 Jul 27.
3
Epigenetic Features in Uterine Leiomyosarcoma and Endometrial Stromal Sarcomas: An Overview of the Literature.
子宫平滑肌肉瘤和子宫内膜间质肉瘤的表观遗传特征:文献综述
Biomedicines. 2022 Oct 13;10(10):2567. doi: 10.3390/biomedicines10102567.
4
Immune activation is essential for the antitumor activity of EZH2 inhibition in urothelial carcinoma.免疫激活对于 EZH2 抑制在尿路上皮癌中的抗肿瘤活性至关重要。
Sci Adv. 2022 Oct 7;8(40):eabo8043. doi: 10.1126/sciadv.abo8043. Epub 2022 Oct 5.
5
Combination of AZD3463 and DZNep Prevents Bone Metastasis of Breast Cancer by Suppressing Akt Signaling.AZD3463与DZNep联合使用通过抑制Akt信号通路预防乳腺癌骨转移。
Front Pharmacol. 2021 May 28;12:652071. doi: 10.3389/fphar.2021.652071. eCollection 2021.
6
The roles of Polycomb repressive complexes in mammalian development and cancer.多梳抑制复合物在哺乳动物发育和癌症中的作用。
Nat Rev Mol Cell Biol. 2021 May;22(5):326-345. doi: 10.1038/s41580-021-00341-1. Epub 2021 Mar 15.
7
MiR-101-3p and Syn-Cal14.1a Synergy in Suppressing EZH2-Induced Progression of Breast Cancer.MiR-101-3p与Syn-Cal14.1a协同抑制EZH2诱导的乳腺癌进展
Onco Targets Ther. 2020 Sep 28;13:9599-9609. doi: 10.2147/OTT.S264600. eCollection 2020.
8
Engaging chromatin: PRC2 structure meets function.结合染色质:PRC2 结构与功能的邂逅。
Br J Cancer. 2020 Feb;122(3):315-328. doi: 10.1038/s41416-019-0615-2. Epub 2019 Nov 11.
9
DZNep inhibits Hif-1α and Wnt signalling molecules to attenuate the proliferation and invasion of BGC-823 gastric cancer cells.DZNep抑制Hif-1α和Wnt信号分子,以减弱BGC-823胃癌细胞的增殖和侵袭。
Oncol Lett. 2019 Oct;18(4):4308-4316. doi: 10.3892/ol.2019.10769. Epub 2019 Aug 22.
10
CATACOMB: An endogenous inducible gene that antagonizes H3K27 methylation activity of Polycomb repressive complex 2 via an H3K27M-like mechanism.CATACOMB:一种内源性诱导基因,通过类似于 H3K27M 的机制拮抗多梳抑制复合物 2 的 H3K27 甲基化活性。
Sci Adv. 2019 Jul 3;5(7):eaax2887. doi: 10.1126/sciadv.aax2887. eCollection 2019 Jul.