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A single amino acid at the PNT domain of ERG mediates its leukemogenic activity through interaction with the NCoR-HDAC3 co-repressor complex.

ABSTRACT: A single amino acid at the PNT domain of ERG mediates its leukemogenic activity through interaction with the NCoR-HDAC3 co-repressor complex.

PROVIDER: PRJNA824433 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18674301.fastq.gz	Fastqsanger.gz
	SRR18674102.fastq.gz	Fastqsanger.gz
	SRR18674302.fastq.gz	Fastqsanger.gz
	SRR18674103.fastq.gz	Fastqsanger.gz
	SRR18674303.fastq.gz	Fastqsanger.gz

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The NCOR-HDAC3 co-repressive complex modulates the leukemogenic potential of ERG.

Project description:The ETS transcription factor ERG is involved in several cancers including leukemia. However, ERG domains and co-factors involved in leukemogenesis remain largely uncharacterized and as a transcription factor it is currently undruggable. Here, we report a critical role for the conserved amino-acid proline at position 199, at the 3’ end of the PNT domain, for ERG’s leukemogenic activity. Specifically, we demonstrate that it is required for ERG-induced self-renewal and restriction of myeloid differentiation in hematopoietic progenitor cells and for initiation of leukemia in mouse transduction/transplantation models. Mechanistically, we show that P199 facilitates the interaction of ERG with the NCoR-HDAC3 co-repressor complex. Inhibition of HDAC3 reduced in vitro and in vivo growth of human ERG-dependent leukemic cells as well as growth of ERG dependent prostate cancer cells. Thus, the interaction of ERG with the NCoR-HDAC3 co-repressor complex is required for its oncogenic activity and modulation of this interaction may provide an opportunity for therapeutic intervention.

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The NCOR-HDAC3 co-repressive complex modulates the leukemogenic potential of the transcription factor ERG.

Project description:The ERG (ETS-related gene) transcription factor is linked to various types of cancer, including leukemia. However, the specific ERG domains and co-factors contributing to leukemogenesis are poorly understood. Drug targeting a transcription factor such as ERG is challenging. Our study reveals the critical role of a conserved amino acid, proline, at position 199, located at the 3' end of the PNT (pointed) domain, in ERG's ability to induce leukemia. P199 is necessary for ERG to promote self-renewal, prevent myeloid differentiation in hematopoietic progenitor cells, and initiate leukemia in mouse models. Here we show that P199 facilitates ERG's interaction with the NCoR-HDAC3 co-repressor complex. Inhibiting HDAC3 reduces the growth of ERG-dependent leukemic and prostate cancer cells, indicating that the interaction between ERG and the NCoR-HDAC3 co-repressor complex is crucial for its oncogenic activity. Thus, targeting this interaction may offer a potential therapeutic intervention.

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