EC-8042 reverses the gained accessibility caused by HDACi in H3K27M-DIPG
Ontology highlight
ABSTRACT: 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. Using ATAC-seq, we identified that HDACi cause heightened accessibility, and the HDACi-opened chromatin regions are highly enriched for SP/KLF motifs. 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 ATAC-seq in SU-DIPG-XVII cells after treated with DMSO, vorinostat and combination vorinostat with EC-8042. And discovered that EC-8042 reverses the gained accessibility caused by HDACi.
ORGANISM(S): Homo sapiens
PROVIDER: GSE255010 | GEO | 2024/02/08
REPOSITORIES: GEO
ACCESS DATA