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Area of Science:

  • Hematology
  • Molecular Biology
  • Cancer Stem Cell Biology

Background:

  • Acute myeloid leukemia (AML) is driven by leukemic stem cells (LSCs) often exhibiting dysregulated Wnt signaling.
  • LEF1, a key Wnt pathway mediator, can induce AML in mice and serves as a prognostic factor in normal karyotype AML.

Purpose of the Study:

  • To investigate the differential expression of LEF1 isoforms in normal hematopoietic stem cells (HSCs) versus AML LSCs.
  • To elucidate the functional roles of distinct LEF1 isoforms in AML pathogenesis and normal stemness.
  • To assess the therapeutic potential of targeting the β-catenin/LEF1 interaction.

Main Methods:

  • Analysis of LEF1 isoform expression in treatment-naïve normal karyotype AML and normal human HSCs.
  • Gene expression profiling and Chromatin Immunoprecipitation Sequencing (ChiP-Seq) in murine models.
  • Functional studies assessing the impact of impairing LEF1/β-catenin binding on cell growth.

Main Results:

  • AML LSCs and cells predominantly express the long, β-catenin-binding LEF1 isoform, whereas normal HSCs express a short, N-terminally truncated isoform lacking this binding site.
  • The long LEF1 isoform is associated with Wnt-β-catenin signaling and oncogenic pathways, while the short isoform correlates with stemness genes.
  • Inhibiting LEF1 binding to β-catenin significantly reduced AML growth but did not affect normal HSCs.

Conclusions:

  • A distinct expression pattern of LEF1 isoforms exists between normal and AML cells.
  • The long LEF1 isoform is crucial for AML propagation and represents a potential therapeutic vulnerability.
  • Targeting the β-catenin/LEF1 interaction offers a promising strategy for selective AML treatment.