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Updated: Jan 10, 2026

Analysis of Retinoic Acid-induced Neural Differentiation of Mouse Embryonic Stem Cells in Two and Three-dimensional Embryoid Bodies
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Balancing Activation and Repression: CoREST-p300 Antagonism Controls Retinoic Acid-Driven Differentiation in AML.

Mina M Tayari1, Helena Gomes Dos Santos1, Sadat Dokaneheifard1

  • 1Sylvester Comprehensive Cancer Center, Department of Human Genetics, University of Miami Miller School of Medicine, Miami, FL, USA.

Biorxiv : the Preprint Server for Biology
|November 24, 2025
PubMed
Summary

Dual inhibition of LSD1/CoREST with Corin and ATRA synergizes to overcome resistance in acute myeloid leukemia (AML). This combination promotes robust myeloid differentiation and apoptosis by reactivating retinoic acid signaling pathways.

Keywords:
HDACLSD1acute myeloid leukemia (AML)differentiation therapyenhancerepigenetic regulationhistone modificationp300

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Prediction and Validation of Gene Regulatory Elements Activated During Retinoic Acid Induced Embryonic Stem Cell Differentiation
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Area of Science:

  • Hematology
  • Epigenetics
  • Molecular Biology

Background:

  • The histone demethylase KDM1A (LSD1) is crucial for hematopoietic differentiation but highly expressed in hematologic malignancies.
  • LSD1 inhibition is a potential strategy to enhance retinoic acid (RA)-responsive gene expression in acute myeloid leukemia (AML).

Purpose of the Study:

  • To investigate the interaction between LSD1 and RAR/RXR heterodimers in AML.
  • To evaluate the efficacy of Corin, a dual LSD1/CoREST inhibitor, in combination with all-trans retinoic acid (ATRA) for AML treatment.

Main Methods:

  • Studied LSD1 interaction with RAR/RXR at genomic loci.
  • Assessed differentiation and apoptosis induction by single-agent and combination therapies (Corin + ATRA).
  • Analyzed H3K4me3 levels, CoREST-RAR/RXR complex disruption, and p300 coactivator recruitment.

Main Results:

  • LSD1 restricts chromatin accessibility and transcriptional activation of differentiation programs in AML.
  • Corin combined with ATRA synergistically induces robust myeloid differentiation and apoptosis.
  • Combination therapy disrupts CoREST-RAR/RXR complexes, enhances p300 recruitment, and shifts chromatin to an active state.

Conclusions:

  • The functional antagonism between CoREST and p300 is a key regulatory axis in RA signaling in AML.
  • Corin and ATRA re-sensitize non-APL AML cells to RA-induced differentiation, offering a therapeutic strategy for ATRA-refractory leukemias.