Abstract 762: Genome-wide mapping of binding sites for the DEK oncoprotein by ChIP-seq.

Abstract

The DEK oncogene is overexpressed in a wide range of cancers, including acute myeloid leukemia (AML). While DEK was initially described as a protein binding to certain topological chromatin structures, recent studies implicate DEK in the epigenetic and transcriptional regulation of specific genes. To assess the global gene binding of DEK, we performed chromatin immunoprecipitation followed by next generation sequencing (ChIP-seq). We demonstrate that DEK does not bind evenly throughout the genome, but rather accumulates around transcription start sites, with binding to promoters and initial parts of the coding sequences. Furthermore, gene set enrichment analysis revealed that DEK preferentially binds genes associated with epigenetic regulation of gene expression. Our results represent the first genome-wide characterization of DEK binding, and further establish DEK as a transcriptional regulator with a specific set of target genes. Citation Format: Carl Sanden, Linnea Järvstråt, Tove Ullmark, Björn Nilsson, Urban Gullberg. Genome-wide mapping of binding sites for the DEK oncoprotein by ChIP-seq. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 762. doi:10.1158/1538-7445.AM2013-762