Study

Glioblastoma initiating cells are sensitive to histone demethylase inhibition due to epigenetic deregulation

Study ID Alternative Stable ID Type
EGAS00001003750 Other

Study Description

Tumor-initiating cells are a subpopulation of cells that have self-renewal capacity to regenerate a tumor. Here, we identify stem cell-like chromatin features in human glioblastoma initiating cells (GICs) and link them to a loss of the repressive histone H3 lysine 9 trimethylation (H3K9me3) mark. Increasing H3K9me3 levels by histone demethylase inhibition led to cell death in GICs but not in their differentiated counterparts. The induction of apoptosis was accompanied by a loss of the activating H3 lysine 9 acetylation (H3K9ac) modification and accumulation of DNA damage and downregulation of DDR genes. Upon knockdown of histone demethylases KDM4C and KDM7A both differentiation and DNA damage was induced. Thus, the H3K9me3-H3K9ac equilibrium is crucial for GIC viability and represents a chromatin feature that can be exploited to specifically target this tumor subpopulation.

Study Datasets 1 dataset.

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Dataset ID Description Technology Samples
EGAD00001005124
ChIP-seq and RNA-seq of glioblastoma initiating cells and their differentiated counterparts with and without inhibition/knockdown of KDMs.
Illumina HiSeq 2000 90

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