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MOZ regulates B-cell progenitors and, consequently, Moz haploinsufficiency dramatically retards MYC-induced lymphoma

Bilal N Sheikh1, Stanley C W Lee1, Farrah El-Saafin1

  • 1The Walter and Eliza Hall Institute of Medical Research, Melbourne, Victoria, Australia; and Department of Medical Biology, and.

Blood
|January 22, 2015
PubMed

Insights

Wild-type MOZ protein is crucial for B-cell progenitor proliferation and hematopoietic malignancy. Inhibiting MOZ may reduce the proliferative capacity of MEIS1 and HOX-driven lymphoma and leukemia cells.

Area of Science:

  • Hematology
  • Molecular Biology
  • Oncology

Background:

  • The histone acetyltransferase MOZ (MYST3, KAT6A) is implicated in aggressive acute myeloid leukemia due to chromosomal translocations.
  • Wild-type MOZ's role in normal B-cell development and its potential contribution to hematopoietic malignancies remain under investigation.

Purpose of the Study:

  • To investigate the function of wild-type MOZ in regulating B-cell progenitor proliferation.
  • To determine MOZ's role in hematopoietic malignancy, specifically in the context of B-cell lymphoma.

Main Methods:

  • Utilized the Eμ-Myc mouse model of aggressive pre-B/B-cell lymphoma.
  • Assessed the impact of Moz haploinsufficiency on mouse survival and B-cell progenitor proliferation.
  • Analyzed gene expression overlap between MOZ, MLL1, and menin, focusing on Meis1 regulation.

Main Results:

  • Loss of one Moz allele significantly increased median survival in the Eμ-Myc lymphoma model (3.9-fold).
  • MOZ is essential for maintaining B-cell progenitor proliferative capacity, even with c-MYC overexpression.
  • B-cell progenitor numbers were reduced in Moz haploinsufficient animals.
  • MOZ directly maintains the expression of genes vital for normal B-cell development, including Meis1.
  • MOZ was found to localize to the Meis1 locus and maintain its expression in pre-B cells.

Conclusions:

  • Wild-type MOZ plays a critical role in maintaining B-cell progenitor proliferation and is involved in hematopoietic malignancy.
  • MOZ's regulation of Meis1 expression is a key mechanism underlying its function in B-cell development and potentially in leukemogenesis.
  • Partial inhibition of MOZ could be a therapeutic strategy against MEIS1 and HOX-driven lymphoma and leukemia.

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