zeste 抑制蛋白增强子 (EZHIP) 通常在生殖细胞发育过程中表达，并在多种癌症中被归类为癌症睾丸抗原 (CTA)。 2020 年，4% 的弥漫性中线神经胶质瘤 (DMG) 被证明异常表达 EZHIP，反映了 DMG 标志性组蛋白 H3 K27M (H3K27M) 癌组蛋白突变。与 H3K27M 类似，EZHIP 是多梳抑制复合物 2 (PRC2) 的负调节因子，导致整体表观基因组重塑。在本观点中，我们探讨了 H3K27M- 和 EZHIP-DMG 之间的相似性和差异，重点是它们共同的 PRC2 抑制功能特征、它们的遗传和表观基因组景观、起源细胞的可能差异以及治疗途径。即将进行的 EZHIP 研究将有助于更好地了解其在胶质瘤发生和 DMG 治疗中的作用。版权所有 © 2024 作者。由爱思唯尔公司出版。保留所有权利。

The enhancer of zeste inhibitory protein (EZHIP) is typically expressed during germ cell development and has been classified as a cancer-testis antigen (CTA) in various cancers. In 2020, 4% of diffuse midline gliomas (DMGs) were shown to aberrantly express EZHIP, mirroring the DMG hallmark histone H3 K27M (H3K27M) oncohistone mutation. Similar to H3K27M, EZHIP is a negative regulator of polycomb repressive complex 2 (PRC2), leading to global epigenomic remodeling. In this opinion, we explore the similarities and disparities between H3K27M- and EZHIP-DMGs with a focus on their shared functional hallmark of PRC2 inhibition, their genetic and epigenomic landscapes, plausible differences in the cell of origin, and therapeutic avenues. Upcoming research on EZHIP will help better understand its role in gliomagenesis and DMG therapy.Copyright © 2024 The Author(s). Published by Elsevier Inc. All rights reserved.