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JMJD1C forms condensate to facilitate a RUNX1-dependent gene expression program shared by multiple types of AML

Qian Chen1, Saisai Wang1, Juqing Zhang2

  • 1State Key Laboratory of Molecular Oncology, School of Basic Medical Sciences, Tsinghua University, Beijing 100084, China.

Protein & Cell
|October 25, 2024
PubMed
Summary
This summary is machine-generated.

Jumonji Domain Containing 1C (JMJD1C) is crucial for acute myeloid leukemia (AML) cell survival. JMJD1C interacts with RUNX1, facilitating a transcriptional program that supports leukemic cell survival across diverse AML subtypes.

Keywords:
JMJD1CRUNX1acute myeloid leukemiaenhancer-promoter interactionenzymatic activity independent functionphase separation

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Area of Science:

  • Hematology
  • Molecular Biology
  • Cancer Research

Background:

  • Jumonji Domain Containing 1C (JMJD1C), a lysine demethylase 3 (KDM3) family member, is essential for acute myeloid leukemia (AML) cell survival.
  • The precise mechanisms by which JMJD1C regulates leukemic programs in various AML subtypes remain largely uncharacterized.

Purpose of the Study:

  • To elucidate the role and mechanism of JMJD1C in regulating leukemic cell survival in acute myeloid leukemia.
  • To investigate the interaction between JMJD1C and the transcription factor RUNX1 in the context of AML.

Main Methods:

  • Co-immunoprecipitation assays to detect protein-protein interactions.
  • Genome-wide localization studies to identify JMJD1C binding sites.
  • Analysis of transcriptional programs regulated by JMJD1C and RUNX1.

Main Results:

  • JMJD1C directly interacts with the master hematopoietic transcription factor RUNX1.
  • JMJD1C is recruited to the genome by RUNX1, facilitating a RUNX1-driven transcriptional program essential for leukemic cell survival.
  • The N-terminal disordered region of JMJD1C is critical for condensate formation and RUNX1 interaction, influencing enhancer-promoter contacts and gene expression.

Conclusions:

  • JMJD1C plays a critical, non-catalytic role in transcriptional regulation within AML.
  • The interaction between JMJD1C and RUNX1 provides a shared mechanism underlying the survival of diverse leukemia types.
  • Targeting JMJD1C represents a potential broad-spectrum therapeutic strategy for AML.