Enhancer of zeste homolog 2 (EZH2) in endocrine tumors: current knowledge and future directions
Recommended Citation
Kumari P, Garg S, Arya AK, Kaur J, Sachdeva NK, Saikia UN, Dahiya D, Bhadada SK, and Rao SD. Enhancer of zeste homolog 2 (EZH2) in endocrine tumors: current knowledge and future directions. Expert Opin Ther Targets 2025; 1-11.
Document Type
Article
Publication Date
3-1-2025
Publication Title
Expert opinion on therapeutic targets
Abstract
INTRODUCTION: Enhancer of zeste homolog 2 (EZH2) is a histone methyltransferase that orchestrates gene expression via epigenetic and non-epigenetic mechanisms. EZH2 performs epigenetic functions by methylating histones and/or non-histone proteins and suppressing or activating target genes. Moreover, non-epigenetic functions involve dysregulation of target genes independent of histone methylation, thereby impacting multiple signaling pathways.
AREAS COVERED: EZH2 has emerged as a pivotal player in the initiation of various cancers. EZH2 overexpression facilitated by H3K27me3 is the principal driver. However, the consequent dysregulation of target genes resulting from EZH2 overexpression has emerged as a secondary instigator of tumorigenesis, leading to metastasis and poor prognosis. Further complexity arises from somatic mutations in EZH2 and downstream target genes such as BRAF and RASSF1A. However, understanding its effects on endocrine tumors/cancers remains an underexplored with the potential to significantly enhance clinical outcomes and contribute to human health. Therefore, the present review focuses on the multifaceted functions of EZH2 and its pathophysiological mechanisms in tumor proliferation, with a specific emphasis on endocrine tumors.
EXPERT OPINION: Investigating EZH2 mechanisms and targeting with inhibitors and drugs is an active area of research that could offer a promising avenue for treatment and a better understanding of molecular therapeutic interventions.
Medical Subject Headings
Humans; Enhancer of Zeste Homolog 2 Protein; Animals; Epigenesis, Genetic; Gene Expression Regulation, Neoplastic; Endocrine Gland Neoplasms; Molecular Targeted Therapy; Prognosis; Mutation; Antineoplastic Agents
PubMed ID
40111060
Volume
29
Issue
3
First Page
159
Last Page
169
