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Gaëlle Cordonnier1, Amit Mandoli2, Nicolas Cagnard3

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The CBFβ-SMMHC oncoprotein interacts with the Polycomb Repressive Complex 1 (PRC1) in acute myeloid leukemia (AML). This interaction alters PRC1 binding and gene expression across the AML genome.

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acute myeloid leukemiacore binding factorepigenetic regulationoncogenepolycomb

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Area of Science:

  • Molecular Biology
  • Cancer Genetics
  • Epigenetics

Background:

  • Mutations in Polycomb Repressive Complex (PRC) components impact tumor biology.
  • The influence of PRC-interacting molecules, like the core binding factor (CBF) complex, on polycomb activity remains largely unknown.

Purpose of the Study:

  • To investigate the interaction between the acute myeloid leukemia (AML)-associated CBFβ-SMMHC fusion oncoprotein and the PRC1 complex.
  • To understand how CBFβ-SMMHC affects polycomb activity and gene regulation in AML.

Main Methods:

  • Investigated the physical interaction and co-localization of CBFβ-SMMHC with PRC1 in AML cells.
  • Utilized depletion of CBFβ-SMMHC to assess changes in genome-wide PRC1 binding and its association with RUNX1.
  • Analyzed gene expression changes, particularly focusing on ribosomal loci.

Main Results:

  • CBFβ-SMMHC physically interacts with and co-localizes with PRC1 across the AML genome, independent of PRC2.
  • Depletion of CBFβ-SMMHC led to increased genome-wide PRC1 binding and altered PRC1-RUNX1 association.
  • PRC1 preferentially associated with actively transcribed genes in CBFβ-SMMHC-expressing cells, and its depletion reduced ribosomal gene transcription.

Conclusions:

  • CBFβ-SMMHC significantly impacts polycomb recruitment and transcriptional regulation in AML.
  • The findings elucidate a novel mechanism by which a fusion oncoprotein influences epigenetic regulation in cancer.