Building on previous work (Fu et al., 2016), we demonstrate the critical role of Sam68 in orchestrating genotoxic stress-initiated NF-κB signaling in the colon and the pathophysiological relevance of Sam68-dependent NF-κB activation in colonic cell survival/recovery from extrinsic DNA damage.

miR-34a prevents inflammation-induced colonic regeneration from oncogenesis by simultaneously targeting processes in both immune and epithelial cells, including T helper 17 cell differentiation, recruitment, and IL-17 induced epithelial proliferation.

Studies of organoid morphogenesis, combined with proteomics and molecular profiling, identify the THBS1-YAP axis as a signalling mechanism that mediates paracrine communication between tumour cells and their wildtype epithelial neighbours.

Human colonic organoid monolayers self organize into regularly spaced stem and differentiated cell compartments, which are maintained by waves of ERK activity originating from extruded/dying cells.

Sestrin2 loss could be a universal mechanism of human colon carcinogenesis that allows for barrier dysfunction, mTORC1 hyperactivation, unrestricted tumor growth and chemoresistance.

Goblet cells secrete mucins—which are key components of mucus—in a process that is regulated by calcium ions, which enter the goblet cells via a mechanism involving a channel protein called TRPM5.

Genetic analyses reveal how CDX2 and BRAF defects seen in serrated colorectal cancer (CRCs), a poor prognosis CRC subset, cooperate in tumorigenesis in humans and in a mouse cancer model.

Colon cancer cells disseminate and colonize distant organ sites along the invasion-metastasis cascade by transiently activating intermediate epithelial to mesenchymal transition states through distinct transcriptional trajectories.

ESRP1 is central to intestinal barrier integrity in mice and humans and alterations in ESRP1 function or expression contribute to intestinal pathology, partly through modified expression of ESRP1-specific GPR137 isoforms.

Proper gut health depends on the balance between two naturally occurring variants of a transcription factor in the colon.