Open chromatin profiling identifies AP1 as a transcriptional regulator in oesophageal adenocarcinoma.
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Britton, E., Rogerson, C., Mehta, S., Li, Y., Li, X., OCCAMS consortium,, Fitzgerald, R., et al. (2017). Open chromatin profiling identifies AP1 as a transcriptional regulator in oesophageal adenocarcinoma.. PLoS genetics, 13 (8), e1006879. https://doi.org/10.1371/journal.pgen.1006879
Oesophageal adenocarcinoma (OAC) is one of the ten most prevalent forms of cancer and is showing a rapid increase in incidence and yet exhibits poor survival rates. Compared to many other common cancers, the molecular changes that occur in this disease are relatively poorly understood. However, genes encoding chromatin remodeling enzymes are frequently mutated in OAC. This is consistent with the emerging concept that cancer cells exhibit reprogramming of their chromatin environment which leads to subsequent changes in their transcriptional profile. Here, we have used ATAC-seq to interrogate the chromatin changes that occur in OAC using both cell lines and patient-derived material. We demonstrate that there are substantial changes in the regulatory chromatin environment in the cancer cells and using this data we have uncovered an important role for ETS and AP1 transcription factors in driving the changes in gene expression found in OAC cells.
OCCAMS consortium, Cell Line, Tumor, Chromatin, Humans, Adenocarcinoma, Esophageal Neoplasms, DNA-Binding Proteins, Adenovirus E1A Proteins, Proto-Oncogene Proteins, Transcription Factors, Transcription Factor AP-1, Chromatin Assembly and Disassembly, Gene Expression Regulation, Neoplastic, Transcriptional Activation, Gene Knockdown Techniques
Our work received funding from the Wellcome Trust (https://wellcome.ac.uk/) the National Institute for Health Research (https://www.nihr.ac.uk/) and Cancer Research UK (http:// www.cancerresearchuk.org/).
Cancer Research UK (15874)
External DOI: https://doi.org/10.1371/journal.pgen.1006879
This record's URL: https://www.repository.cam.ac.uk/handle/1810/284506
Attribution 4.0 International
Licence URL: https://creativecommons.org/licenses/by/4.0/