Global Histone H3 lysine 4 trimethylation (H3K4me3) landscape changes in response to TGF-ß1

We performed Chromatin-Immunoprecipitation followed by Next-Generation Sequencing (ChIP-Seq) in PC-3 Cells stimulated with TGF-ß1 for different duration. We used anti-H3K4me3 antibody to immunoprecipitate DNA fragment associated with H3K4me3. We found that a number of regions associated with H3K4me3 increased in a time-dependent manner upon TGF-ß1 stimulation. Further the regions were classified into different Functional annotations. Overall design: TGF-ß play a critical role in Epithelial to Mesenchymal Transition (EMT) in different types of cancers. TGF- ß can exhibit pro and anti-tumour activities in cancer cells in a context and microenvironment dependent manner. On the hand epigenetic modifications are increasingly playing an important role in various cellular processes. Aberration in epigenetic processes can lead to disruption in different gene functions and malignant cellular transformation. There is a growing interest in understanding the role of H3K4me3 in cancer survival. Investigation on the epigenetic reprogramming during the TGF- ß induced EMT, found a global reduction in the heterochromatin mark H3 Lys9 dimethylation (H3K9me2), an increase in the euchromatin mark H3 Lys4 trimethylation (H3K4me3) and an increase in the transcriptional mark H3 Lys36 trimethylation (H3K36me3). As TGF-ß and H3K4me3 plays an important role in tumorigenesis, our study focuses on finding globally, H3K4me3 associated regions in response to TGF-ß. ChIP-Seq was performed in Prostate cancer cells (PC-3) to understand the involvement and mechanism of H3K4me3 modification in TGF-ß induced EMT.