Epithelial-mesenchymal transition (EMT) is a fundamental developmental program, which is believed to be reactivated during the progression of in situ carcinoma to aggressive metastatic cancers. Ras-ERK pathway has been shown to play a crucial role in EMT. We have previously shown that ERK2, but not ERK1, is necessary for RasV12-induced EMT and overexpression of ERK2 is sufficient to promote EMT. ERK2 promotes EMT by regulating several factors, including the upregulation of transcription factors ZEB1/2. ZEB1/2 repress expression of E-cadherin, which is necessary for polar epithelial tissue formations.
