Breast cancer is the leading cause of cancer-related morbidity and mortality in women. Despite improvements in diagnostic and therapeutic tools, we still lack effective treatment regimens for advanced stages of breast cancer. Cellular plasticity, the ability of a cell to switch cell identities, often becomes de-regulated and heightened in aggressive cancer cells. This is believed to fuel intra-tumoural heterogeneity, metastasis, and resistance to therapy, which are the main drivers of poor outcomes in breast cancer patients.
Changes in cell identity can be achieved through epigenetic plasticity, which describes how easily the epigenome can change in response to stimuli. An example of epigenetic plasticity is bivalent chromatin, where tri-methylation of lysine 4 on histone 3 (H3K4me3) and tri-methylation of lysine 27 on histone 3 (H3K27me3) co-exist on the same nucleosome. In embryonic stem cells, bivalent chromatin is known to poise lineage-specific genes for future activation or repression. Bivalent chromatin has been implicated in breast cancer tumourigenesis and therapy resistance. However, the dynamics of bivalent chromatin in breast cancer remain poorly understood. Here, we present profiles of bivalent chromatin in breast cancer cell lines as an essential first step towards uncovering the role of bivalent chromatin in breast cancer.