Exploring Epigenetic Changes in the Development of Gemcitabine Resistance [AsPC1R_vs_AsPC1_CUTTAG]. Exploring Epigenetic Changes in the Development of Gemcitabine Resistance [AsPC1R_vs_AsPC1_CUTTAG]

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). Overall design: To establish gemcitabine-resistant (Gem-R) PDAC cell lines, a progressive exposure to increasing concentrations of gemcitabine was employed. High-throughput epigenome technique CUT&Tag-seq was utilized for comprehensive exploration of epigenetic landscapes.