Transcriptional Regulator CNOT3 Defines an Aggressive Colorectal Cancer Subtype.

ABSTRACT: Cancer cells exhibit dramatic alterations of chromatin organization at cis-regulatory elements, but the molecular basis, extent, and impact of these alterations are still being unraveled. Here, we identify extensive genome-wide modification of sites bearing the active histone mark H3K4me2 in primary human colorectal cancers, as compared with corresponding benign precursor adenomas. Modification of certain colorectal cancer sites highlighted the activity of the transcription factor CNOT3, which is known to control self-renewal of embryonic stem cells (ESC). In primary colorectal cancer cells, we observed a scattered pattern of CNOT3 expression, as might be expected for a tumor-initiating cell marker. Colorectal cancer cells exhibited nuclear and cytoplasmic expression of CNOT3, suggesting p

SUBMITTER: Cejas P 

PROVIDER: S-EPMC5290184 | biostudies-literature | 2017 Feb

REPOSITORIES: biostudies-literature