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Updated: Jun 8, 2025

Induction and Analysis of Epithelial to Mesenchymal Transition

Induction and Analysis of Epithelial to Mesenchymal Transition

Published on: August 27, 2013

在宫癌中,CCL22/CCR4的激活导致EMT过程在EZH2-介导的表观遗传调节下重塑

Li Zhang¹, Sijuan Tian¹, Jie Chang¹

¹Department of Gynecology and Obstetrics, the First Affiliated Hospital of Xi'an Jiaotong University, No.277 West Yanta Road, Xi'an 710061, China.

Journal of Cancer

|November 8, 2024

概括

增强体同类2 (EZH2) 的增强剂通过DNA甲基转移酶3A (DNMT3A) 通过表观基因激活化基因 (C-C动机) 连接体22 (CCL22) 和其受体 (CCR4),促进宫癌的进展和上皮细胞转化为介质细胞转化 (EMT).

科学领域:

表观遗传学和癌症生物学
分子瘤学分子瘤学
宫癌的发病原因宫癌的发病原因

背景情况:

宫癌 (CC) 在全球范围内对女性构成重大公共卫生挑战.
影响基因表达的表观遗传修饰与CC发展有关.
化学因子 (C-C动机) 配体22 (CCL22) 和它的受体CC-化学因子受体4 (CCR4) 与瘤进展和转移有关.

研究的目的:

为了研究增强肠胃同源2 (EZH2) 在宫癌中CCL22/CCR4表达的表观遗传调节中的作用.
阐明EZH2在CC中影响表皮细胞转移到介质细胞转换 (EMT) 的机制.
确定DNA甲基转移酶3A (DNMT3A) 在EZH2介导的CCL22/CCR4调节中的参与.

主要方法:

对CCL22和CCR4表达和促进体DNA甲基化在CC组织与正常宫组织中的分析.
在体外和体内测试以评估DNMT3A与CCL22和CCR4促进体区域的结合.
在CC细胞系中抑制EZH2和DNMT3A,以评估它们对基因表达,甲基化和细胞迁移的影响.
抑制CCL22蛋白质以评估其对细胞迁移和EMT标记物的影响.

主要成果:

在CC组织中,CCL22和CCR4被显著上调,促进体DNA甲基化增加.
脱甲基化重新激活了CCL22和CCR4转录,而EZH2下调导致促进体甲基化增加,并通过DNMT3A减少了CCL22/CCR4的mRNA表达.
EZH2和DNMT3A静止受差异影响的细胞迁移和EMT标记物 (vimentin,slug,牛,β-catenin,ZO-1),与CCL22抑制减少迁移和EMT.

结论:

EZH2通过DNMT3A在表观遗传上激活CCL22/CCR4表达,有助于EMT和宫癌的进展.
针对EZH2/DNMT3A/CCL22/CCR4轴可能为宫癌提供治疗策略.

关键词:

在CCL22-CCR4中.在DNMT3A中,它是DNMT3A.在EMT中,EMT是EMT.在 EZH2 中使用.宫癌:子宫癌是一种癌症.

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