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EC-8042 disrupts both the primary SP/KLF transcription regulatory network and the secondary network induced by HDACi treatment. [H3K27me3 ChIP-seq]

ABSTRACT: EC-8042 disrupts both the primary SP/KLF transcription regulatory network and the secondary network induced by HDACi treatment. [H3K27me3 ChIP-seq]

PROVIDER: PRJNA1114698 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29127817_1.fastq.gz	Fastqsanger.gz
	SRR29127817_2.fastq.gz	Fastqsanger.gz
	SRR31377647_1.fastq.gz	Fastqsanger.gz
	SRR31377647_2.fastq.gz	Fastqsanger.gz
	SRR31377648_1.fastq.gz	Fastqsanger.gz

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EC-8042 disrupts both the primary SP/KLF transcription regulatory network and the secondary network induced by HDACi treatment. [ATAC-seq]

Project description:Diffuse intrinsic pontine gliomas (DIPGs), frequently harboring H3K27M mutations, are lethal pediatric brain tumors within no effective treatment. By performing ATAC-seq in human pontine progenitor cells (hPPCs) and H3K27M-mutated DIPG cells, we identified that the DIPG-opened chromatin regions are highly enriched for SP/KLF motifs. We show that SP1 depletion or inhibition of SP/KLF DNA binding with EC-8042, an optimized Mithramycin analog, significantly suppresses the proliferation and invasiveness of H3K27M-DIPG cells. In a screen of epigenetic drugs, we find that histone deacetylase inhibitors (HDACi) synergize with EC-8042 to suppress H3K27M-DIPG cell growth. We then performed ATAC-seq in SU-DIPG-XVII cells after treated with DMSO, EC-8042, vorinostat and combination vorinostat with EC-8042. And discovered that HDACi treatment enhances chromatin accessibility to SP/KLF factors, while EC-8042 disrupts both the primary SP/KLF transcription regulatory network and the secondary network induced by HDACi treatment.

2025-02-20 | GSE268109 | GEO

EC-8042 disrupts both the primary SP/KLF transcription regulatory network and the secondary network induced by HDACi treatment. [SP1&H3K27me3 CUT&Tag]

Project description:Diffuse intrinsic pontine gliomas (DIPGs), frequently harboring H3K27M mutations, are lethal pediatric brain tumors within no effective treatment. The DIPG-opened chromatin regions are proved to be highly enriched for SP/KLF motifs. Using CUT&Tag of SP1 and H3K27me3 in human pontine progenitor cells (hPPCs) and H3K27M-mutated DIPG cells, we detected the gain of SP1 occupancy correlates with the loss of H3K27me3. Here our epigenomic analyses uncover a marked enrichment of the SP/KLF transcription factors in open chromatin regions specifically in H3K27M-mutated DIPG cells compared to normal pontine neural progenitor cells. We show that SP1 depletion or inhibition of SP/KLF DNA binding with EC-8042, an optimized Mithramycin analog, significantly suppresses the proliferation and invasiveness of H3K27M-DIPG cells. In a screen of epigenetic drugs, we find that histone deacetylase inhibitors (HDACi) synergize with EC-8042 to suppress H3K27M-DIPG cell growth. CUT&Tag of SP1 in SU-DIPG-XVII cells after treated with DMSO, EC-8042, vorinostat and combination vorinostat with EC-8042 revealed that HDACi treatment enhances chromatin accessibility to SP/KLF factors, while EC-8042 disrupts both the primary SP/KLF transcription regulatory network and the secondary network induced by HDACi treatment.

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EC-8042 disrupts both the primary SP/KLF transcription regulatory network and the secondary network induced by HDACi treatment. [H3K27me3 ChIP-seq]

Project description:Diffuse intrinsic pontine gliomas (DIPGs) are lethal pediatric brain tumors with limited therapeutic options. Frequently harboring H3K27M mutations, these tumors are resistant to Histone deacetylase inhibitors (HDACi) in clinical trials for yet unclear reasons. Given this, there is a critical need for exploring the reasons of insufficient clinical manifestations of HDACi and identifying effective combinatorial therapeutic strategy for the treatment of DIPG. To explore the possibility of combining HDACi with EC-8042, an analog of Mithramycin that blocks the DNA binding of SP/KLF factors，We performed ChIP-seq of H3K27me3 in SU-DIPG-XVII cells after treated with DMSO, EC-8042, vorinostat and combination vorinostat with EC-8042. And discovered that EC-8042 reverses the activated transcriptional programs caused by HDACi.

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EC-8042 disrupts both the primary SP/KLF transcription regulatory network and the secondary network induced by HDACi treatment. [ATAC-seq]

Project description:EC-8042 disrupts both the primary SP/KLF transcription regulatory network and the secondary network induced by HDACi treatment. [ATAC-seq]

| PRJNA1114697 | ENA

EC-8042 disrupts both the primary SP/KLF transcription regulatory network and the secondary network induced by HDACi treatment. [SP1&H3K27me3 CUT&Tag]

Project description:EC-8042 disrupts both the primary SP/KLF transcription regulatory network and the secondary network induced by HDACi treatment. [SP1&H3K27me3 CUT&Tag]

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Inhibition of SP/KLF transcription regulatory network and histone deacetylases acts synergistically against H3K27M-DIPG

Project description:Diffuse intrinsic pontine gliomas (DIPGs), frequently harboring H3K27M mutations, are lethal pediatric brain tumors within no effective treatment. Here our epigenomic analyses uncover a marked enrichment of the SP/KLF transcription factors in open chromatin regions specifically in H3K27M-mutated DIPG cells compared to normal pontine neural progenitor cells. We show that SP1 depletion or inhibition of SP/KLF DNA binding with EC-8042, an optimized Mithramycin analog, significantly suppresses the proliferation and invasiveness of H3K27M-DIPG cells. In a screen of epigenetic drugs, we find that histone deacetylase inhibitors (HDACi) synergize with EC-8042 to suppress H3K27M-DIPG cell growth. The RNA-seq in SU-DIPG-IV and SU-DIPG-XVII cells after treated with DMSO, EC-8042, vorinostat and combination vorinostat with EC-8042 revealed that HDACi activates transcriptional programs that enhance tumor adaptability and invasiveness, an effect counteracted by EC-8042. And EC-8042 in combination with HDACi synergistically represses the expression of cell cycle-associated genes and therefore suppresses H3K27M-DIPG cell proliferation, inhibiting tumor progression in orthotopic xenograft models. Transcriptomic analysis further supports that the combination treatment drives transcriptional programs correlating with favorable prognosis in DIPG patients. Therefore, our regulome profiling in H3K27M-DIPGs has provided mechanistic insights into HDACi resistance and a proof-of-concept for novel targeting therapeutics.

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Inhibition of SP/KLF transcription regulatory network and histone deacetylases acts synergistically against H3K27M-DIPG

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