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Genome-wide identification of DOT1L-regulated targets via H3K79me2 modification in SW1990 pancreatic cancer cells

ABSTRACT: Disruption of epigenetic regulation plays a pivotal role in pancreatic cancer progression, yet the genome-wide targets of DOT1L-mediated histone H3 lysine 79 dimethylation (H3K79me2) remain poorly defined. In this study, we investigated the epigenetic landscape regulated by DOT1L in SW1990 pancreatic ductal adenocarcinoma cells. Cells were treated with EPZ-5676, a selective DOT1L inhibitor, or vehicle control, followed by chromatin immunoprecipitation sequencing (ChIP-seq) using an H3K79me2-specific antibody. We identified differentially enriched regions between EPZ-5676-treated and untreated cells, reflecting global loss of H3K79me2 upon DOT1L inhibition. Integration with gene annotation data revealed putative DOT1L-regulated genes involved in transcriptional regulation, cell proliferation, and cancer signaling pathways. These findings provide insight into the role of DOT1L in maintaining the active chromatin state and transcriptional programs in pancreatic cancer cells and highlight potential therapeutic targets in epigenetic intervention.

ORGANISM(S): Homo sapiens

PROVIDER: GSE303754 | GEO | 2026/07/28

REPOSITORIES: GEO

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