SRA

Chromatin architecture is essential to transcriptional regulation. Cancer cells undergo critical chromatin remodeling processes that interact with the activation or silencing of oncogenes or tumor suppressor genes. These processes, together with other alterations of the functional status of chromatins, are characterized by epigenetic marks such as covalent histone modifications, DNA methylations and etc. The epigenetic landscapes defined by these marks are key to understand their regulatory mechanisms as well as the contributions to cancer onset and progression. In this study, we focus on defining the epigenetics landscapes across different breast cancer subtypes. Here we present a collection of 11 key histone modifications across 13 distinct breast cancer cell lines, representing 5 major breast cancer subtypes, including two ER positive subtypes: Lumina-A and Lumina-B, HER2 positive subtype and triple-negative subtypes TNBC-Basal and TNBC-ClaudinLow, as well as normal-like immortal breast cells. Using combinatorial patterns of multiple histone modifications, we defined the whole genome chromatin state maps and identified specific signatures in breast cancer subtypes. Overall design: H3K4me1, H3K4me3, H3K27me3, H3K36me3, H3K9me3, H3K9ac, H3K79me2, H3K27ac, H2BK120ub1, H3K23ac, and H4K8ac ChIP-seq, and input in 76NF2V, MCF10A, MCF7, ZR751, MB361, UACC812, SKBR3, AU565, HCC1954, MB231, MB436, MB468, and HCC1937 cells.