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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]

GSE268111 Homo sapiens Genome binding/occupancy profiling by high throughput sequencing 9 samples Submitted 2025/02/20 Platform GPL24676
Summary
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.
Published in
Targeting the SP/KLF Transcriptional Regulatory Network Synergizes with HDAC Inhibition to Impede Progression of H3K27M Diffuse Intrinsic Pontine Glioma
Kong Y, Wang F, Jing R et al. · Cancer research 2025 · PMID 40053472 · doi:10.1158/0008-5472.CAN-24-2227
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Also filed as BioProject PRJNA1114698 and SRA study SRP509209. Searching any of these in the dataset finder brings you back here.

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