Abstract
Enhancer of zeste homolog 2 (EZH2) is a histone-lysine N-methyltransferase that encrypts a member of the Polycomb group (PcG) family. EZH2 forms a repressive chromatin structure which eventually participates in regulating the development as well as lineage propagation of stem cells and glioma progression. Posttranslational modifications are distinct approaches for the adjusted modification of EZH2 in the development of cancer. The amino acid succession of EZH2 protein makes it appropriate for covalent modifications, like phosphorylation, acetylation, O-GlcNAcylation, methylation, ubiquitination, and sumoylation. The glioma microenvironment is a dynamic component that comprises, besides glioma cells and glioma stem cells, a complex network that comprises diverse cell types like endothelial cells, astrocytes, and microglia as well as stromal components, soluble factors, and the extracellular membrane. EZH2 is well recognized as an essential modulator of cell invasion as well as metastasis in glioma. EZH2 oversecretion was implicated in the malfunction of several fundamental signaling pathways like Wnt/β-catenin signaling, Ras and NF-κB signaling, PI3K/AKT signaling, β-adrenergic receptor signaling, and bone morphogenetic protein as well as NOTCH signaling pathways. EZH2 was more secreted in glioblastoma multiforme than in low-grade gliomas as well as extremely secreted in U251 and U87 human glioma cells. Thus, the blockade of EZH2 expression in glioma could be of therapeutic value for patients with glioma. The suppression of EZH2 gene secretion was capable of reversing temozolomide resistance in patients with glioma. EZH2 is a promising therapeutic as well as prognostic biomarker for the treatment of glioma.
Highlights
Gliomas are primary brain malignant tumors which are often triggered by malignant modification of neural stem cells, progenitor cells, and differentiated glial cells such as astrocyte, oligodendrocyte, and ependymal cells [1,2,3,4]
Enhancer of zeste homolog 2 (EZH2) oversecretion was implicated in the malfunction of several fundamental signaling pathways like the wingless-related integration site (Wnt)/β-catenin signaling, rat sarcoma (Ras) and NF-κB signaling pathways, phosphoinositide 3kinase (PI3K)/AKT pathway, β-adrenergic receptor signaling, and bone morphogenetic protein (BMP) as well as NOTCH signaling pathways in cancers [16, 96,97,98,99]
It was established that EZH2 was more secreted in Glioblastoma multiforme (GBM) than in low-grade gliomas as well as extremely secreted in U87 human glioma cells [42]
Summary
Gliomas are primary brain malignant tumors which are often triggered by malignant modification of neural stem cells, progenitor cells, and differentiated glial cells such as astrocyte, oligodendrocyte, and ependymal cells [1,2,3,4] These lesions are histologically grouped into Grades I-IV according to the World Health Organization (WHO) criteria [4, 5]. Grade III comprises astrocytoma or anaplastic astrocytoma based on histological classification [4]. They are depicted with hypercellularity, nuclear atypia, and mitotic characters [4]. Search parameters were EZH2 and/or the posttranslational modifications, microenvironment, signaling pathways, biomarker, and therapy in gliomas
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