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Updated: Oct 2, 2025
A Method to Study de novo Formation of Chromatin Domains
Published on: August 23, 2019
An overview of the development of EED inhibitors to disable the PRC2 function
Kai-Lu Liu1, Kongkai Zhu1, Hua Zhang1
1School of Biological Science and Technology, University of Jinan Jinan 250022 China hkhhh.k@163.com bio_zhangh@ujn.edu.cn.
Abstract:
Polycomb repressive complex 2 (PRC2) catalyzes the methylation of histone H3 lysine 27 (H3K27) and the enrichment of its catalytic product H3K27me3 is responsible for the silencing of tumor suppressor genes and the blocking of transcripts related to immunity and cell terminal differentiation. Aberrations of PRC2 components, such as mutation and overexpression, have been observed in various cancers, which makes PRC2 a potential therapeutic target for cancer. Up to now, targeting the enhancer of zeste homolog 2 (EZH2), the catalytic subunit of PRC2, represents the main strategy in the development of PRC2 inhibitors. Although significant progress has been made, new problems also emerge, e.g. the drug resistance caused by secondary mutations. In recent years, more and more efforts have shifted to another new strategy - targeting embryonic ectoderm development (EED) to disrupt its major interactions with other components, which are necessary to the PRC2 function, and some promising results have been obtained. This review summarizes the recent development of EED inhibitors as possible chemotherapy for cancer treatment, which could help accelerate future related research work.
Insights
Targeting embryonic ectoderm development (EED) offers a new strategy against cancer by inhibiting Polycomb repressive complex 2 (PRC2). This approach aims to overcome drug resistance associated with targeting EZH2, a key PRC2 component.
Area of Science:
- Epigenetics
- Cancer Biology
- Drug Discovery
Background:
- Polycomb repressive complex 2 (PRC2) regulates gene expression through histone methylation (H3K27me3), impacting tumor suppressor genes, immunity, and cell differentiation.
- PRC2 component aberrations are linked to various cancers, establishing PRC2 as a significant therapeutic target.
- Current PRC2 inhibitor strategies primarily target the catalytic subunit, enhancer of zeste homolog 2 (EZH2), but face challenges like drug resistance due to secondary mutations.
Purpose of the Study:
- To review recent advancements in developing embryonic ectoderm development (EED) inhibitors as a novel therapeutic strategy for cancer.
- To highlight the potential of targeting EED to disrupt PRC2 function and overcome existing therapeutic limitations.
Main Methods:
- Literature review of recent research on EED inhibitors and their mechanisms of action.
- Analysis of preclinical data and emerging therapeutic strategies targeting PRC2 components.
Main Results:
- Emerging evidence suggests targeting EED is a promising alternative to EZH2 inhibition for PRC2-targeted cancer therapy.
- EED inhibition disrupts essential PRC2 complex interactions, offering a potential route to circumvent drug resistance.
Conclusions:
- Targeting EED represents a novel and promising strategy for developing new cancer chemotherapies.
- Further research into EED inhibitors could accelerate the development of effective treatments for various cancers.
