Genome-wide chromatin accessibility, DNA methylation and gene expression analysis of histone deacetylase inhibition in triple-negative breast cancer

摘要

Triple-negative breast cancer (TNBC), especially the subset with a basal phenotype, represents the most aggressive subtype of breast cancer. Unlike other solid tumors, TNBCs harbor a low number of driver mutations. Conversely, we and others have demonstrated a significant impact of epigenetic alterations, including DNA methylation and histone post-translational modifications, affecting TNBCs. Due to the promising results in pre-clinical studies, histone deacetylase inhibitors (HDACi) are currently being tested in several clinical trials for breast cancer and other solid tumors. However, the genome-wide epigenetic and transcriptomic implications of HDAC inhibition are still poorly understood. Here, we provide detailed information about the design of a multi-platform dataset that describes the epigenomic and transcriptomic effects of HDACi. This dataset includes genome-wide chromatin accessibility (assessed by ATAC-Sequencing), DNA methylation (assessed by Illumina HM450K BeadChip) and gene expression (assessed by RNA-Sequencing) analyses before and after HDACi treatment of HCC1806 and MDA-MB-231, two human TNBC cell lines with basal-like phenotype. prs.rt("abs_end"); Specifications Organism/cell line/tissue Homo sapiens / cancer cell lines (HCC1806 and MDA-MB-231 ) Sex Female Sequencer or array type - Illumina HiSeq 2500 - Illumina HumanMethylation450 BeadChip Data format Raw ( FASTQ ) and analyzed ( BigWig ) for ATAC sequencing data Raw ( FASTQ ) and analyzed ( TXT ) for RNA sequencing data Raw ( IDAT ) and analyzed ( TXT ) for DNA methylation arrays data Experimental factors Human triple-negative cell lines treated with HDAC inhibitor ( LBH589 ) Experimental features HCC1806 and MDA-MB-231 treated with 10?nM of LBH589 for 28?days Consent N / A Sample source location N / A Full-size table Table options.