Genomics

Dataset Information

144

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


ABSTRACT: 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

INSTRUMENT(S): Illumina HiSeq 2000 (Homo sapiens)

SUBMITTER: Nikos Kourtis  

PROVIDER: GSE90716 | GEO | 2018-03-20

REPOSITORIES: GEO

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Publications


Cellular transformation is accompanied by extensive rewiring of many biological processes leading to augmented levels of distinct types of cellular stress, including proteotoxic stress. Cancer cells critically depend on stress-relief pathways for their survival. However, the mechanisms underlying the transcriptional initiation and maintenance of the oncogenic stress response remain elusive. Here, we show that the expression of heat shock transcription factor 1 (HSF1) and the downstream mediators  ...[more]

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