Metabolic adaptations underlie epigenetic vulnerabilities in chemoresistant breast cancer. [ChIP-Seq]

Purpose:Assess the reprogramming of H3K4me1, H3K4me3, H3K27ac and H3K27me3 in paclitaxel-resistant triple-negative breast cancer cells relative to paclitaxel-sensitive cells Methods: ChIP-seq was performed on paclitaxel-treated MDA-MB-436 cells that are resistant to Paclitaxel (R20A, R20B, R20C) and in control-treated (DMSO) parental MDA-MB-436 cells that are sensitive to Paclitaxel (DMSO) Results: Using we mapped about 20 million sequence reads per sample to the human genome (hg19) and identified significant peaks in each cell lines using MACS.2.0 tool. Conclusions: Our study identified major reprogramming of H3K27me3 in the taxol-resistant TNBC cells relative to parental (TNBC cells), with loss of discrete H3K27me3 peaks in the resistant cells concomittent to acquisition of clusters of H3K27me3. ChIP-seq was performed on paclitaxel-treated MDA-MB-436 cells that are resistant to Paclitaxel (R20A, R20B, R20C) and in control-treated (DMSO) parental MDA-MB-436 cells that are sensitive to Paclitaxel (DMSO)