The chromatin accessibility change by PRC2 inactivation with or without IFNγ stimulation in human MPNST cancer cells

PRC2-isogenic human malignant peripheral nerve sheath tumor (MPNST) M3 cells were generated through CRISPR/Cas9-mediated knockout of the PRC2 core component, SUZ12. PRC2 loss led to not only significant increase, but also significant decrease of chromatin accessibility at 15,346 (16% of all ATAC peaks) and 20,099 genomic loci (21% of all ATAC peaks), respectively. PRC2 loss decreased the chromatin accessibility for IFNγ-responsive loci in M3 cells, resulting in dampened response to IFNγ stimulation. PRC2-isogenic human MPNST M3 cells (sgCon, sgSUZ12) were treated with PBS or 10 ng/ml IFNγ stimulation for 24 hr, followed by chromatin accessibility profiling.