Role of enhancer activation in pancreatic cancer metastasis

Aberrancies in chromatin conformation can lead to altered gene expression thus promoting cancer development. Chromatin is the substratum for transcription factors (TF) to bind DNA and the degree of chromatin compaction determines TF accessibility to their target cis-regulatory elements including promoters and enhancers. Results comparing chromatin profiles between primary tumors and matched non-malignant tissues evidence a profound dynamic throughout the carcinogenic process (1-4). This dynamic effectively reprograms the enhancer landscape toward the activation of oncogenes such as MYC (1,2). Supporting findings in a variety of tumors of different lineages suggest that the aberrant enhancer reprogramming is a general mechanism involved in carcinogenesis (1-4). However, the role that this mechanism could have in the metastatic process remains vastly unexplored