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The epithelial–mesenchymal transition ( EMT ) is a crucial morphological event that occurs during progression of epithelial tumors. We reported previously that levels of the δ‐crystallin/E2‐box factor 1 (δ EF 1) family proteins (Zinc finger E‐box binding homeobox 1 [ ZEB 1]/δ EF 1 and  ZEB 2/ Smad‐interacting protein 1), key regulators of the  EMT , are positively correlated with  EMT  phenotypes and aggressiveness of breast cancer. Here, we show that Ets1 induces  ZEB  expression and activates the   ZEB 1  promoter, independently of its threonine 38 phosphorylation status. In the basal‐like subtype of breast cancer cells, si RNA s targeting Ets1 repressed expression of  ZEB s and partially restored their epithelial phenotypes and sensitivity to antitumor drugs. Epithelium‐specific  ETS  transcription factor 1 ( ESE 1), a member of the Ets transcription factor family, was originally characterized as being expressed in an epithelial‐restricted pattern, placing it within the epithelium‐specific  ETS  subfamily.  ESE 1, highly expressed in the luminal subtype of breast cancer cells, was repressed by activation of the  MEK – ERK  pathway, resulting in induction of  ZEB s through Ets1 upregulation. Conversely, Ets1, highly expressed in the basal‐like subtype, was repressed by inactivation of  MEK – ERK  pathway, resulting in reduction of  ZEB s through  ESE 1 upregulation. These findings suggest that  ESE 1 and Ets1, whose expressions are reciprocally regulated by the  MEK – ERK  pathway, define the  EMT  phenotype through controlling expression of  ZEB s in each subtype of breast cancer cells.

Ets1 and ESE1 reciprocally regulate expression of ZEB1/ZEB2, dependent on ERK1/2 activity, in breast cancer cells