SMAD1/5 signaling is essential for the full transforming growth factor β (TGF-β)-induced transcriptional program and physiological responses and is induced via a novel receptor activation mechanism, involving two distinct type I receptors.

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.

Integrated live cell imaging and image analyses in the framework of transition path theories identify epithelial-to-mesenchymal transition proceeds through parallel paths.

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.

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.

Genetic mouse models and human cell lines show that Musashi proteins promote an epithelial/luminal state and inhibit epithelial–mesenchymal transition (EMT), and genome-wide maps of translational regulatory targets connect Musashi proteins to an epithelial alternative splicing program and to the regulation of EMT.

Overexpression of PLK1 triggers oncogenic transformation and transcriptional reprogramming of prostate epithelial cells, which stimulates cell migration and invasion.

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

The inhibition of colorectal cancer (CRC) proliferation, migration, and invasion is attributed to BEST4, which exhibits epistasis over Hes4 in the downregulation of Twist1 and consequent suppression of epithelial-to-mesenchymal transition in CRC.

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.