scispace - formally typeset
Open AccessJournal ArticleDOI

Targeted Disruption of the EZH2/EED Complex Inhibits EZH2-dependent Cancer

Reads0
Chats0
TLDR
By dissociating the EZH2/EED complex, this work pharmacologically modulates an epigenetic “writer” and suppress PRC2-dependent cancer cell growth.
Abstract
Enhancer of zeste homolog 2 (EZH2) is the histone lysine N-methyltransferase component of the Polycomb repressive complex 2 (PRC2), which, in conjunction with embryonic ectoderm development (EED) and suppressor of zeste 12 homolog, regulates cell lineage determination and homeostasis. Enzymatic hyperactivity has been linked to aberrant repression of tumor suppressor genes in diverse cancers. Here, we report the development of stabilized α-helix of EZH2 (SAH-EZH2) peptides that selectively inhibit H3 Lys27 trimethylation by dose-responsively disrupting the EZH2-EED complex and reducing EZH2 protein levels, a mechanism distinct from that reported for small-molecule EZH2 inhibitors targeting the enzyme catalytic domain. MLL-AF9 leukemia cells, which are dependent on PRC2, undergo growth arrest and monocyte-macrophage differentiation upon treatment with SAH-EZH2, consistent with observed changes in expression of PRC2-regulated, lineage-specific marker genes. Thus, by dissociating the EZH2-EED complex, we pharmacologically modulate an epigenetic 'writer' and suppress PRC2-dependent cancer cell growth.

read more

Content maybe subject to copyright    Report

Citations
More filters
Journal ArticleDOI

Targeting EZH2 in cancer

TL;DR: A unifying perspective is synthesized that the promotion of cancer arises from disruption of the role of EZH2 as a master regulator of transcription.
Journal ArticleDOI

Discovery of cancer drug targets by CRISPR-Cas9 screening of protein domains

TL;DR: It is shown that the magnitude of negative selection can be used to infer the functional importance of individual protein domains of interest, and a broader application of this approach may allow comprehensive identification of protein domains that sustain cancer cells and are suitable for drug targeting.
Journal ArticleDOI

Hydrocarbon-Stapled Peptides: Principles, Practice, and Progress

TL;DR: The more than decade-long experience in developing stapled peptides as biomedical research tools and prototype therapeutics is described, highlighting lessons learned, pitfalls to avoid, and keys to success.
Journal ArticleDOI

Structure-Based Design of Inhibitors of Protein-Protein Interactions: Mimicking Peptide Binding Epitopes

TL;DR: A new classification of peptidomimetics (classes A–D) is introduced that enables a clear assignment of available approaches for the structure-based design of PPI inhibitors through stabilizing or mimicking turns, β-sheets, and helices.
Journal ArticleDOI

Epigenetic balance of gene expression by Polycomb and COMPASS families.

TL;DR: The balance between the prototypic chromatin modifiers Polycomb and COMPASS complexes and their role in gene regulation and normal development is reviewed, with evidence supporting a role for these complexes in tumor progression.
References
More filters
Journal ArticleDOI

Identification of human brain tumour initiating cells

TL;DR: The development of a xenograft assay that identified human brain tumour initiating cells that initiate tumours in vivo gives strong support for the CSC hypothesis as the basis for many solid tumours, and establishes a previously unidentified cellular target for more effective cancer therapies.
Journal ArticleDOI

Theoretical Basis, Experimental Design, and Computerized Simulation of Synergism and Antagonism in Drug Combination Studies

TL;DR: The median-effect principle and its mass-action law based computer software are gaining increased applications in biomedical sciences, from how to effectively evaluate a single compound or entity to how to beneficially use multiple drugs or modalities in combination therapies.
Journal ArticleDOI

Role of Histone H3 Lysine 27 Methylation in Polycomb-Group Silencing

TL;DR: The purification and characterization of an EED-EZH2 complex, the human counterpart of the Drosophila ESC-E(Z) complex, is reported, and it is demonstrated that the complex specifically methylates nucleosomal histone H3 at lysine 27 (H3-K27).
Journal ArticleDOI

The polycomb group protein EZH2 is involved in progression of prostate cancer

TL;DR: Dysregulated expression of EZH2 may be involved in the progression of prostate cancer, as well as being a marker that distinguishes indolent prostate cancer from those at risk of lethal progression.
Journal ArticleDOI

Histone methyltransferase activity associated with a human multiprotein complex containing the Enhancer of Zeste protein

TL;DR: The isolation of a multiprotein E(z) complex that contains extra sex combs, suppressor of zeste-12, and the histone binding proteins RbAp46/RbAp48 is reported, which possesses HMT activity with specificity for Lys 9 (K9) and Lys 27 (K27) of histone H3.
Related Papers (5)