Epithelial–mesenchymal transition

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.

With the emergence of increasingly potent androgen deprivation therapy, rates of treatment-emergent small-cell neuroendocrine prostate cancer are increasing. In a recent prospective study, Aggarwal and colleagues defined the frequency and clinical and genomic characteristics of these tumours.

The roles of transforming growth factor β (TGF-β) depend on the cellular context. Paraspeckle component 1 now arises as a driver of epithelial-to-mesenchymal transition and stemness transcription factors to redirect effectors from tumour suppressive to pro-metastatic gene promoters, emerging as a contextual determinant of TGF-β function.