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E-cad Promotes the Primed Pluripotent State

Transition from the naïve to the primed state of pluripotency associates with the epithelial to mesenchymal transition (EMT) and a metabolic switch from oxidative phosphorylation to glycolysis, which are both hallmarks of oncogenic transformation. Moreover, loss of E‐cadherin (E‐cad) junctions represents an early event of EMT during the exit from pluripotency and cellular transformation. Now, a new STEM CELLS study from researchers led by Aseel M. Sharaireh (University of Manchester, UK) has established that E‐cad inhibition leads to profound alterations in the proteome of mouse embryonic stem cells, with a metabolic switch indicative of a naïve-to-primed state transition centralized around EP300. E‐cad is a target of the transcriptional coactivator EP300 and suggests the existence of a disruptive feedback loop relevant to the maintenance of pluripotency and oncogenesis.