The study investigates the role of the Notch signaling pathway in epithelial-to-mesenchymal transition (EMT) during cardiac development and oncogenic transformation. Notch activity is shown to promote EMT by inducing the expression of the Snail repressor, a key mediator of EMT. In the embryonic heart, Notch functions via lateral induction to promote a TGFβ-mediated EMT that leads to the cellularization of developing cardiac valvular primordia. In zebrafish embryos, transient ectopic expression of activated Notch1 (N11C) results in hypercellular cardiac valves, while Notch inhibition prevents valve development. Overexpression of N11C in immortalized endothelial cells in vitro induces EMT and oncogenic transformation, accompanied by increased Snail expression and reduced VE-cadherin expression. The findings suggest that Notch plays a crucial role in both normal cardiac development and tumor progression by promoting EMT through the induction of Snail.The study investigates the role of the Notch signaling pathway in epithelial-to-mesenchymal transition (EMT) during cardiac development and oncogenic transformation. Notch activity is shown to promote EMT by inducing the expression of the Snail repressor, a key mediator of EMT. In the embryonic heart, Notch functions via lateral induction to promote a TGFβ-mediated EMT that leads to the cellularization of developing cardiac valvular primordia. In zebrafish embryos, transient ectopic expression of activated Notch1 (N11C) results in hypercellular cardiac valves, while Notch inhibition prevents valve development. Overexpression of N11C in immortalized endothelial cells in vitro induces EMT and oncogenic transformation, accompanied by increased Snail expression and reduced VE-cadherin expression. The findings suggest that Notch plays a crucial role in both normal cardiac development and tumor progression by promoting EMT through the induction of Snail.