Regulation of histone H3K27 methylation in inflammation and cancer.

IF 6.3 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY
Jing Ma, Yalin Zhang, Jingyuan Li, Yanqi Dang, Dan Hu
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Abstract

Inflammation is a multifaceted defense mechanism of the immune system against infection. Chronic inflammation is intricately linked to all stages of tumorigenesis and is therefore associated with an elevated risk of developing serious cancers. Epigenetic mechanisms have the capacity to trigger inflammation as well as facilitate tumor development and transformation within an inflammatory context. They achieve this by dynamically modulating the expression of both pro-inflammatory and anti-inflammatory cytokines, which in turn sustains chronic inflammation. The aberrant epigenetic landscape reconfigures the transcriptional programs of inflammatory and oncogenic genes. This reconfiguration is pivotal in dictating the biological functions of both tumor cells and immune cells. Aberrant histone H3 lysine 27 site (H3K27) methylation has been shown to be involved in biological behaviors such as inflammation development, tumor progression, and immune response. The establishment and maintenance of this repressive epigenetic mark is dependent on the involvement of the responsible histone modifying enzymes enhancer of zeste homologue 2 (EZH2), jumonji domain containing 3 (JMJD3) and ubiquitously transcribed tetratricopeptide repeat gene X (UTX) as well as multiple cofactors. In addition, specific pharmacological agents have been shown to modulate H3K27 methylation levels, thereby modulating inflammation and carcinogenesis. This review comprehensively summarises the current characteristics and clinical significance of epigenetic regulation of H3K27 methylation in the context of inflammatory response and tumor progression.

组蛋白H3K27甲基化在炎症和癌症中的调控。
炎症是免疫系统对抗感染的多方面防御机制。慢性炎症与肿瘤发生的所有阶段都有复杂的联系,因此与发展成严重癌症的风险增加有关。表观遗传机制具有触发炎症以及促进炎症环境下肿瘤发展和转化的能力。它们通过动态调节促炎和抗炎细胞因子的表达来实现这一目标,而促炎和抗炎细胞因子反过来又维持慢性炎症。异常的表观遗传景观重新配置了炎症和致癌基因的转录程序。这种重组在决定肿瘤细胞和免疫细胞的生物学功能方面是关键的。异常组蛋白H3赖氨酸27位点(H3K27)甲基化已被证明与炎症发展、肿瘤进展和免疫反应等生物学行为有关。这一抑制性表观遗传标记的建立和维持依赖于zeste同源物2 (EZH2)、jumonji结构域3 (JMJD3)和泛在转录的四肽重复基因X (UTX)以及多种辅助因子的参与。此外,特定的药物已被证明可以调节H3K27甲基化水平,从而调节炎症和致癌作用。本文综述了H3K27甲基化在炎症反应和肿瘤进展中的表观遗传调控的现状及临床意义。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
CiteScore
6.30
自引率
0.00%
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0
审稿时长
10 weeks
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