GEO series
Exploring Epigenetic Changes in the Development of Gemcitabine Resistance [AsPC1R_vs_AsPC1_CUTTAG]
GSE247161
Homo sapiens
Genome binding/occupancy profiling by high throughput sequencing
11 samples
2024/09/23
GPL24676
Summary
To elucidate the epigenetic events, particularly the dynamic alterations in chromatin states during the development of gemcitabine resistance in pancreatic cancer cells, both the parental AsPC1 cells and the gemcitabine-resistant counterparts, AsPC1R cells, were employed for mapping of the histone modification landscape. The CUT&Tag-seq technology was used for precise detection of histone marks, including H3K4me1 (associated with enhancers), H3K27ac (related to active enhancers and promoters), H3K4me3 (linked to PolII-bound and CpG-rich promoters), H3K9me3 (associated with heterochromatin regions), and H3K27me3 (indicative of Polycomb inhibition).
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