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Regulation of Hematopoietic Stem Cells

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All blood and immune cells are produced from the multipotent hematopoietic stem cells (HSCs) by the process of hematopoiesis. However, they all have a limited life span. In addition, many are depleted in immune surveillance or combatting an injury or infection. This makes blood one of the most regenerative tissues. Hematopoiesis helps replenish these blood and immune cells, restoring the body's normal functioning. However, overproduction of blood and immune cells can make them cancerous or...

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SWI/SNF Blockade Disrupts PU.1-Directed Enhancer Programs in Normal Hematopoietic Cells and Acute Myeloid Leukemia.

Courtney Chambers^1,2,3, Katerina Cermakova^1,2, Yuen San Chan^1,2

¹Department of Molecular and Cellular Biology, Center for Precision Environmental Health, Baylor College of Medicine, Houston, Texas.

Cancer Research

|January 20, 2023

Summary

SWI/SNF inhibition in acute myeloid leukemia (AML) disrupts PU.1 (SPI1) enhancer programs, causing leukemic cell differentiation. This therapy shows therapeutic promise but also induces off-tumor effects like leukopenia in normal immune cells.

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Area of Science:

Hematology
Cancer Biology
Chromatin Biology

Background:

SWI/SNF chromatin remodeling complexes are crucial for maintaining leukemic identity in acute myeloid leukemia (AML) by regulating MYC expression.
The role of the hematopoietic transcription factor PU.1 (SPI1) and its interaction with SWI/SNF in AML and normal hematopoiesis remains incompletely understood due to PU.1's pioneer-like activity.

Purpose of the Study:

To elucidate the interplay between PU.1 and SWI/SNF in AML and normal hematopoiesis.
To investigate the therapeutic potential and off-tumor effects of SWI/SNF inhibition in AML.

Main Methods:

Analysis of PU.1 binding and SWI/SNF recruitment in AML cells.
Assessment of DNA accessibility and core regulatory factor binding upon SWI/SNF inhibition.
Evaluation of SWI/SNF inhibition effects on normal hematopoietic cell populations (B cells, monocytes).
Testing SWI/SNF inhibition efficacy in an immunocompetent AML mouse model and human AML samples.

Main Results:

PU.1 primarily binds targets independently of SWI/SNF, recruiting SWI/SNF to facilitate accessibility for other factors like RUNX1, LMO2, and MEIS1.
SWI/SNF inhibition in AML cells reduced DNA accessibility and core factor binding at PU.1 sites, leading to PU.1 redistribution.
Similar effects were observed in normal hematopoietic cells, impairing PU.1-dependent B-cell and monocyte populations.
SWI/SNF inhibition demonstrated significant therapeutic responses in AML models, promoting differentiation and reducing leukemic stem cells, but also caused leukopenia.

Conclusions:

SWI/SNF inhibition disrupts PU.1-directed enhancer programs, leading to AML cell differentiation and potential therapeutic benefits.
The study reveals significant on- and off-tumor effects of SWI/SNF blockade, including leukopenia in normal PU.1-dependent immune cells.
A variable therapeutic window for SWI/SNF blockade in AML exists, necessitating careful consideration of its impact on normal hematopoiesis and immune function.