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HOXA9 Reprograms the Enhancer Landscape to Promote Leukemogenesis.

Yuqing Sun1, Bo Zhou1, Fengbiao Mao1

  • 1Department of Pathology, University of Michigan Medical School, Ann Arbor, MI 48109, USA.

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|October 2, 2018
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Summary
This summary is machine-generated.

Overexpression of HOXA9 in acute leukemia drives enhancer reorganization and activates embryonic genes. Targeting HOXA9-dependent enhancer changes offers a potential therapeutic strategy for this cancer.

Keywords:
HOXA9KMT2MLLacute leukemiade novo enhancerepigeneticshistone methylationpioneer factortranscription factor

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Area of Science:

  • Molecular Biology
  • Cancer Biology
  • Epigenetics

Background:

  • Aberrant HOXA9 expression is a hallmark of acute leukemia.
  • HOXA9 drives leukemogenesis through various oncogenic pathways.

Purpose of the Study:

  • To investigate the role of HOXA9 in enhancer reorganization in acute leukemia.
  • To elucidate the molecular mechanisms by which HOXA9 alters the enhancer landscape and gene expression.

Main Methods:

  • Analysis of enhancer landscape changes in myeloid and B progenitor cells with HOXA9 overexpression.
  • Chromatin immunoprecipitation (ChIP) assays to identify transcription factor binding and histone modifications.
  • Genetic deletion of MLL3/MLL4 to assess their role in HOXA9-mediated leukemogenesis.
  • In vivo leukemogenesis studies.

Main Results:

  • HOXA9 overexpression induces significant enhancer reorganization, creating de novo enhancers specific to leukemia.
  • These alterations activate an ectopic embryonic gene program.
  • HOXA9 acts as a pioneer factor at de novo enhancers, recruiting CEBPα and the MLL3/MLL4 complex.
  • Deletion of MLL3/MLL4 prevents histone H3K4 methylation at de novo enhancers and inhibits leukemogenesis.

Conclusions:

  • HOXA9 orchestrates enhancer reorganization, leading to aberrant gene activation in acute leukemia.
  • The MLL3/MLL4 complex is crucial for HOXA9-mediated enhancer function and leukemogenesis.
  • Targeting HOXA9-driven enhancer alterations presents a promising therapeutic avenue for acute leukemia.