Glioblastoma (GBM) is the most common primary brain tumor in adults, and the most lethal form of glioma, characterized by variable histopathology, aggressiveness and poor clinical outcome and prognosis. GBMs constitute a challenge for oncologists because of their molecular heterogeneity, extensive invasion, and tendency to relapse.

Glioma cells demonstrate a variety of deregulated genomic pathways and extensive interplay with epigenetic alterations. Epigenetic modifications have emerged as essential players in GBM research, with biomarker potential for tumor classification and prognosis and for drug targeting. Histone posttranslational modifications (PTMs) are crucial regulators of chromatin architecture and gene expression, playing a pivotal role in malignant transformation, tumor development and progression.

Alteration in the expression of genes coding for lysine and arginine methyltransferases (G9a, SUV39H1 and SETDB1) and acetyltransferases and deacetylases (KAT6A, SIRT2, SIRT7, HDAC4, 6, 9) contribute to GBM pathogenesis. In addition, proteins of the sumoylation pathway are upregulated in GBM cell lines, including E1 (SAE1), E2 (Ubc9) components, and a SUMO-specific protease (SENP1).

Preclinical and clinical studies are currently in progress targeting epigenetic enzymes in gliomas, including a new generation of histone deacetylase (HDAC), protein arginine methyltransferase (PRMT) and bromodomain (BRD) inhibitors. Herein, we provide an update on recent advances in glioma epigenetic research, focusing on the role of histone modifications and the use of epigenetic therapy as a valid treatment option for glioblastoma.

胶质母细胞瘤 (GBM) 是成人最常见的原发性脑肿瘤，也是最致命的胶质瘤形式，其特点是组织病理学、侵袭性和临床结果和预后差。GBMs 对肿瘤学家构成挑战，因为它们的分子异质性、广泛侵袭和复发倾向。

神经胶质瘤细胞表现出多种失调的基因组途径以及与表观遗传改变的广泛相互作用。表观遗传修饰已成为 GBM 研究的重要参与者，具有用于肿瘤分类和预后以及药物靶向的生物标志物潜力。组蛋白翻译后修饰 (PTM) 是染色质结构和基因表达的关键调节因子，在恶性转化、肿瘤发展和进展中发挥着关键作用。

编码赖氨酸和精氨酸甲基转移酶（G9a、SUV39H1 和 SETDB1）以及乙酰转移酶和脱乙酰酶（KAT6A、SIRT2、SIRT7、HDAC4、6、9）的基因表达的改变有助于 GBM 发病机制。此外，在 GBM 细胞系中，SUMO 化途径的蛋白质上调，包括 E1 (SAE1)、E2 (Ubc9) 成分和 SUMO 特异性蛋白酶 (SENP1)。

目前正在进行针对胶质瘤表观遗传酶的临床前和临床研究，包括新一代组蛋白脱乙酰酶 (HDAC)、蛋白质精氨酸甲基转移酶 (PRMT) 和溴结构域 (BRD) 抑制剂。在此，我们提供了关于胶质瘤表观遗传学研究的最新进展，重点关注组蛋白修饰的作用以及表观遗传疗法作为胶质母细胞瘤的有效治疗选择的应用。