Epithelial–mesenchymal transition articles from across Nature Portfolio

Adherens junctions (AJs) are canonical mediators of cell–cell adhesion that support embryonic development and tissue homeostasis. This Review discusses how the properties and behaviours of embryonic tissues emerge from the collective molecular interactions that occur at AJs.

Epithelial–mesenchymal transition (EMT) is crucial in embryogenesis and can be exploited by cancer cells to gain metastatic abilities. A hallmark of EMT is E-cadherin loss. In 2000, Snail was reported as the first E-cadherin repressor identified in the context of EMT, advancing our understanding of embryonic development and cancer progression.

Blanpain and colleagues provide evidence that the small RHO GTPase, RHOJ, mediates resistance to chemotherapy in tumour cells that have undergone epithelial-to-mesenchymal transition by enabling these cells to tolerate replicative stress and promote DNA damage repair.

Bracken and Goodall discuss why epithelial–mesenchymal transition (EMT) has so many regulators, but also consider whether many of these may be ‘false positives’.

Epithelial–mesenchymal transition (EMT) is crucial for development, and for dissemination and invasion of cancer cells. A study now identifies the apical–basolateral polarity status of epithelia as a checkpoint for EMT induction and tumour metastasis through aPKC–Par3-regulated degradation of the EMT transcription factor SNAI1.

D’Amico et al. show that, in the presence of oncogenic RAS mutations, STAT3 acts as a tumour modifier by regulating the epithelial differentiation of pancreatic and lung cancer cells via p63.