National Cancer Institute, Subdirection of Basic Research, Laboratory of Epigenetic and Environment, Av. San Fernando #22 Col. Seccion XVI. Delegacion Tlalpan, C.P 14080 Mexico City, United States.
National Cancer Institute, Subdirection of Basic Research, Laboratory of Carcinogenesis, Av. San Fernando #22 Col. Seccion XVI. Delegacion Tlalpan, C.P 14080 Mexico City, United States.
CNS Neurol Disord Drug Targets. 2017;16(10):1090-1098. doi: 10.2174/1871527317666180110124645.
BACKGROUND & OBJECTIVE: Gliomas constitute 81% of malignant brain tumors and exhibit a poor prognosis. Two main events involved in the progression of gliomas are the deregulation of genes via genetic events and the cellular damage resulting from the formation of reactive oxygen species (ROS). In gliomas, epigenetic abnormalities implicated in the deregulation of deoxyribonucleic acid (DNA) methylation, nucleosome rearrangement, and acetylation of histones, have been depicted. The overproduction of ROS has been implicated in the promotion of these modifications.
In this review, we discuss the epigenetic mechanisms and oxidative events that impact gene silencing and its association with the establishment and development of gliomas. Some of these epigenetic marks, or their related proteins, are under investigation for their potential use as biomarkers in clinical trials to propose personalized therapies for patients with glioblastoma.
脑胶质瘤占恶性脑肿瘤的 81%,预后不良。胶质瘤进展过程中涉及两个主要事件:一是遗传事件导致基因失调,二是活性氧(ROS)形成导致细胞损伤。在脑胶质瘤中,已描述了涉及脱氧核糖核酸(DNA)甲基化、核小体重排和组蛋白乙酰化的基因调控异常的表观遗传异常。ROS 的过度产生被认为促进了这些修饰。
在这篇综述中,我们讨论了影响基因沉默的表观遗传机制和氧化事件,以及其与脑胶质瘤的发生和发展的关系。其中一些表观遗传标记物或其相关蛋白正在被研究,以期将其作为临床试验中的生物标志物,为胶质母细胞瘤患者提出个性化治疗方案。