DKK2 is crucial for the development of lysozyme-expressing cancer cells with Paneth cell characteristics necessary for liver metastasized colon cancer growth.

Resting natural killer cells promote the progress of colon cancer liver metastasis (CCLM), which may be exploited for novel strategies to improve therapeutic outcomes for patients with CCLM.

A novel long non-coding RNA targets microRNA miR-34a for epigenetic silencing and initiates asymmetric division of colon cancer stem cells.

The identification of alternative splicing targets and upstream RNA-binding proteins that underlie EMT and metastasis in colon cancer stratifies patients according to their overall survival and provide new insights on the function of specific isoforms along the migrating cancer stem cell sequence.

Editors' Summary: This Replication Study has reproduced important parts of the original paper.

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.

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.

Leukemia-Related Protein 16 (LRP16), a member of the macro domain family, plays a crucial role in orchestrating genotoxicity-initiated NF-κB signaling in the colon and the pathophysiological relevance of NF-κB activation induced by LRP16 in colonic cell survival/recovery from extrinsic DNA damage.

A key Ras-driven signaling pathway stimulates the preferential translation of an effector, EPSTI1, that is both necessary and sufficient for the epithelial-to-mesenchymal transition-like phenotype in colorectal cancer cells.