Open chromatin profiling identifies AP1 as a transcriptional regulator in oesophageal adenocarcinoma.
Edward BrittonConnor RogersonShaveta MehtaYaoyong LiXiaodun Linull nullRebecca C FitzgeraldYeng S AngAndrew D SharrocksPublished in: PLoS genetics (2017)
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.
Keyphrases
- transcription factor
- gene expression
- genome wide
- genome wide identification
- dna binding
- dna methylation
- squamous cell carcinoma
- dna damage
- single cell
- induced apoptosis
- papillary thyroid
- locally advanced
- electronic health record
- cell death
- cell cycle arrest
- squamous cell
- deep learning
- cell proliferation
- single molecule
- data analysis
- loop mediated isothermal amplification