Project description:MCF-7 (Estrogen receptor positive breast cancer) cells were treated with p300 KAT inhibitor A-485 and genome wide H3K27ac deposition was measured by ChIP-seq.
Project description:Upregulation of enhancer of zeste 2 polycomb repressive complex 2 subunit (EZH2) and its associated histone H3 lysine 27 (H3K27) trimethylation frequently occur in human cancer, yet both preclinical and clinical evidence suggested the very limited benefit of EZH2-targeted therapies. This study investigated the underlying mechanisms from a perspective of EZH2 inhibition-caused histone modification crosstalk. A mass spectrometry approach enabled us discovering the alteration of global histone modifications responding to EZH2 inhibition. Feedback upregulation of H3K27 acetylation (H3K27ac) level is closely associated with limited drug response to EZH2 inhibition across multiple cancer types. H3K27ac alteration caused transcriptional activation of oncoproteins confers drug resistant to EZH2 inhibition. Here we used ChIP-Seq analysis to identify the alteration of genome-wide H3K27ac bingding sites with EZH2 inhibitor treatment in human cancer cell lines.
Project description:Previously, we have shown that HIST1H2ac is overexpressed in MCF-7 breast cancer cell line. It acts as a master regulator of estrogen receptor alpha-dependent gene expression in ER+ breast cancer cells. In the present study, we investigate the genome-wide protein DNA-binding events of HIST1H2ac protein in MCF-7 breast cancer cell line by over-expressing hemagglutinin (HA)-tagged HIST1H2ac and compared with MCF-7 cells over-expressing HA. The protein-bound DNA was recovered by immunoprecipitation using anti-HA antibody. The ChIP DNA and input DNA were sequenced with an Illumina HiSeq 2000 sequencer.
Project description:Identification of genome-wide PRDM16 binding, H3K27ac and H3K4me in WT and Prdm16 conditional knock-out (cKO) mouse (Emx1Ires-Cre; Prdm16flox/flox) at embryonic day 15.5.