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Proliferation and Differentiation of Murine Myeloid Precursor 32D/G-CSF-R Cells

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Published on: February 21, 2018

Enhanced FLI1 accessibility mediates STAG2-mutant leukemogenesis.

Jane J Xu, Viviana Scoca, Yi Chen

Biorxiv : the Preprint Server for Biology

|April 16, 2025

Summary

This summary is machine-generated.

Loss of STAG2 in hematopoietic stem cells increases accessibility to FLI1 targets, driving leukemia development. This altered chromatin architecture co-opts FLI1 signaling, promoting leukemogenesis and sensitivity to MENIN inhibition.

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Area of Science:

Hematology
Cancer Biology
Epigenetics

Background:

Transcription factors (TFs) regulate cell fate and can be dysregulated in cancer.
FLI1 is vital for hematopoietic stem/progenitor cell (HSPC) function, with STAG2 controlling its target accessibility.
STAG2 depletion enhances HSPC self-renewal, but its role in leukemia is not fully understood.

Purpose of the Study:

To investigate the role of STAG2 loss in maintaining FLI1 target accessibility and its impact on leukemic transformation.
To elucidate how altered chromatin architecture co-opts oncogenic TF signaling in STAG2-mutant leukemia.

Main Methods:

Utilized murine models (Stag2/Npm1c/+) to study leukemogenesis.
Analyzed chromatin accessibility, TF binding (FLI1, MENIN), and gene expression in HSPCs and leukemia cells.
Examined immunophenotypes in murine models and human leukemia patients.

Main Results:

STAG2 loss maintains FLI1 target accessibility in HSPCs and enhances FLI1 binding in NPM1c leukemia.
Myeloid-biased HSPCs with increased FLI1 accessibility serve as reservoirs for transformation, leading to fully penetrant leukemia.
STAG2-deficient NPM1c cells show increased chromatin accessibility and looping of stem/leukemia genes, with enrichment for CD34+ immunophenotype in patients.
STAG2-deficient cells exhibit increased chromatin-bound MENIN and heightened sensitivity to MENIN inhibition.

Conclusions:

Enhanced FLI1 chromatin accessibility is a key driver of stemness and leukemic transformation in STAG2-mutant leukemia.
Altered chromatin architecture can co-opt oncogenic TF activity (FLI1) to drive leukemia development and influence therapeutic response.
STAG2 loss promotes leukemogenesis by increasing FLI1 accessibility and conferring sensitivity to MENIN inhibition.