Hijacking of stress response machinery by oncogenes in acute leukaemia [ChIP-seq]. Homo sapiens

HSF1 orchestrates the heat shock response pathway. This pathway is co-opted in cancer and provides critical stress relief from oncogenic stress. HSF1 has a diverse occupancy signature depending on the cell type. In this study, we performed HSF1 ChIP-seq analysis using the human T-ALL cell line CUTLL1 and P12. These results revealed the HSF1 chromatin binding signature in CUTLL1 and P12 cells. MYC is a driving oncogene in T-ALL. The non-oncogene addiction pathways that act downstream of this transcription factor to support anabolic pathways are not well-understood. For this reason, we performed MYC ChIP-seq analysis using the human T-ALL cell line CUTLL1. These results revealed that HSF1 and HSF1 targets are included in the MYC binding signature. Overall design: Twenty million cells were used for the ChIP and precipitated using 5 micrograms of antibody (cell signaling, 4356) against human HSF1. Twenty million cells were used for the ChIP and precipitated using 5 micrograms of antibody (santa cruz biotechnology, N-262) against human MYC

热休克因子1（Heat Shock Factor 1, HSF1）调控热休克反应通路。该通路在癌症中被劫持，可为肿瘤细胞提供关键的致癌应激缓解作用。HSF1的染色质结合特征谱因细胞类型而异。

本研究使用人T细胞急性淋巴细胞白血病（T-cell Acute Lymphoblastic Leukemia, T-ALL）细胞系CUTLL1与P12，开展了HSF1的染色质免疫共沉淀测序（Chromatin Immunoprecipitation Sequencing, ChIP-seq）分析，结果揭示了CUTLL1与P12细胞中HSF1的染色质结合特征谱。

MYC是T-ALL中的驱动性致癌基因。目前对于该转录因子下游支持合成代谢通路的非致癌基因成瘾通路，尚未得到充分阐释。基于此，本研究使用人T-ALL细胞系CUTLL1开展了MYC的ChIP-seq分析，结果显示HSF1及其靶基因均包含于MYC的结合特征谱中。

实验整体设计：
针对人HSF1的ChIP实验：取2000万细胞，以5微克抗人HSF1抗体（Cell Signaling Technology，货号4356）进行免疫沉淀。
针对人MYC的ChIP实验：取2000万细胞，以5微克抗人MYC抗体（Santa Cruz Biotechnology，货号N-262）进行免疫沉淀。