Project description:Chromatin openness is a good indicator of non-coding regulatory elements. Here, we generated ATAC-seq of 8 breast cancer cell lines covering different breast cancer subtypes as an overview of the open chromatin landscapes.
Project description: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.
Project description:The architecture of chromatin specifies eukaryotic cell identity by controlling transcription factor access to sites of gene regulation. Here we describe a dual transposase/peroxidase approach, integrative DNA And Protein Tagging (iDAPT), which detects both DNA (iDAPT-seq) and protein (iDAPT-MS) associated with accessible regions of chromatin. In addition to direct identification of bound transcription factors, iDAPT enables the inference of their gene regulatory networks, protein interactors, and regulation of chromatin accessibility. We applied iDAPT to profile the epigenomic consequences of granulocytic differentiation of acute promyelocytic leukemia, yielding previously undescribed mechanistic insights with potential therapeutic implications. Our findings demonstrate the power of iDAPT as a discovery platform for both the dynamic epigenomic landscapes and their transcription factor components associated with biological phenomena and disease.
Project description:We performed ATAC-seq on publicly available leukemia cell-lines and used them to predict non-coding regulatory mutations in open-chromatin regions of the genome.
Project description:We employed FAIRE-seq to identify open chromatin in head and neck squamous cell carcinoma (HNSCC) patient-derived primary and lymph node cell lines. We further analysed this data to identify differential open chromatin between primary and metastatic cells.