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Related Experiment Video

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Investigation of Genetic Dependencies Using CRISPR-Cas9-based Competition Assays

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Published on: January 7, 2019

Polycomb repressive complex 2 is required for MLL-AF9 leukemia.

Tobias Neff¹, Amit U Sinha, Michael J Kluk

¹Dana-Farber/Children's Hospital Cancer Center, Boston, MA 02115, USA.

Proceedings of the National Academy of Sciences of the United States of America

|March 8, 2012

Summary

This summary is machine-generated.

Polycomb repressive complex 2 (PRC2) plays a role in acute myeloid leukemia (AML) progression. While not essential for initial leukemia growth, inhibiting Ezh2 impacts AML progression and gene expression, suggesting therapeutic potential.

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Investigation of the Transcriptional Role of a RUNX1 Intronic Silencer by CRISPR/Cas9 Ribonucleoprotein in Acute Myeloid Leukemia Cells

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Published on: September 1, 2019

Area of Science:

Epigenetics
Cancer Biology
Hematology

Background:

Epigenetic mechanisms, including Polycomb repressive complex 2 (PRC2), are increasingly recognized for their role in cancer.
PRC2 components are overexpressed in many cancers, but their precise function in cancer development and progression is not fully understood.

Purpose of the Study:

To investigate the role of PRC2 function in leukemia development and progression using conditional alleles for enhancer of zeste 2 (Ezh2) and embryonic ectoderm development (Eed).

Main Methods:

Conditional knockout alleles for Ezh2 and Eed were used in MLL-AF9-mediated acute myeloid leukemia (AML) models.
Leukemia progression was assessed via secondary transplantation assays.
Genome-wide analyses of H3K27me3 and gene expression arrays were performed.

Main Results:

Ezh2-null AML showed impaired acceleration upon secondary transplantation but retained self-renewal capacity.
Partial compensation of Ezh2 loss by Ezh1 was observed, indicated by locus-specific H3K27me3 persistence.
Inactivation of Eed led to complete PRC2 loss and was incompatible with leukemia growth, causing more profound gene expression changes than Ezh2 inactivation.

Conclusions:

Ezh2 is not strictly required for MLL-AF9 AML initiation but contributes to leukemia progression.
Eed is essential for PRC2 function and leukemia viability.
Targeting PRC2 function presents a potential therapeutic strategy for AML.