Enhancer landscapes in chidamide-resistant and chidamide-sensitive cells
NKTL
To investigate the underlying mechanism of resistance to chidamide in NKTL cells, we performed chromatin immunoprecipitation sequencing (ChIP-seq) for H3K27ac and H3K4me3 in two resistant cell lines (HANK1 and SNK6) and two sensitive cell lines (KHYG1 and MEC04). Epigenetic changes in H3K27ac and H3K4me3, which are associated with gene enhancers and promoters, respectively, have been shown to modulate gene activities and confer resistance to drug treatment [Chromatin and transcriptomic profiling of chidamide-resistant and chidamide-sensitive NKTL cells. To gain further insights into the altered transcriptional pathways resulting from epigenetic dysregulation, RNA-seq was performed in two chidamide-resistant (HANK1 and SNK6) and two chidamide-sensitive (KHYG1 and MEC04) cell lines. Integrative transcriptomic and chromatin profiling analyses revealed that the differential H3K27ac peaks were positively correlated with gene expression in NKTL cells (Fig. 