Investigation of regulatory network topology reveals latent design principles of multistable phenotypic landscape.

Inhibiting the RiBi pathway impedes both EMT and MET processes, enhancing chemotherapy efficacy and presenting a novel avenue to tackle advanced breast cancer treatment resistance.

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.

Epithelial to mesenchymal transition (EMT) is a continuous process, in which the transition or intermediate states can be molecularly and spatially defined, shedding new light on development and disease EMT.

Splicing by QKI and RBFOX1 regulates the function of the actin-binding protein FLNB by creating an isoform frequently observed in human cancers that dictates tumor cell plasticity.

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.

Cancer stem cells that have undergone EMT are identified in the region surrounding metastatic human oral tumours in a retrospective cohort study, and these are predictive of metastatic outcome in an image-based machine learning approach.

Erlotinib-resistant AXL overexpressing cells are present in therapy-naive tumors, and expression of AXL in these cells is regulated through a stochastic mechanism centered on the epigenetic regulation of miR-335.

Novel modelling strategies can integrate the dynamics of processes regulating the intestinal epithelium at multiple scales in homeostasis and following perturbations to provide unprecedented insights into the biology of the epithelium and support the development of safer novel drug candidates.

In chick skeletal muscle, an incoming signal leads to two interdependent outcomes: a cell fate change and an epithelial-mesenchymal transition.