In addition to ERs major role in proliferation, it also appears to have established a foothold on repressing EMT activation  by suppressing signal transduction cascades such as TGFβ and NF-κB. [9] This impedes the growth-inhibiting and EMT-promoting effects of the TGFβ cascade and favor the epithelial phenotype but also accelerate cancer cell growth, both known effects of ERα signaling in breast cancer. Changes in TGFβ signaling between normal and cancerous ER-positive cells have been proposed to explain differences in their proliferation status but may also explain the EMT suppressing effect of ERα in ER-positive cancers.[10] Another mechanism through which ER suppresses the induction of EMT  is through suppressing the NF-κB sub-unit RelB expression axis a major EMT inducer.  [11] 

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Our work with the FOXC1 TF highlights the importance of ER as a transcriptional driver suppressing EMT and the negative consequences of diminishing estrogen dependent ER activation abrogating the suppression of EMT resulting in an aggressive, invasive phenotype,  acquired tamoxifen resistance, and eventually leading to recurrence and metastasis.