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Epithelial-to-Mesenchymal Transition (EMT) has long been considered to be critical for the development of lung metastasis in breast cancer [1]. Cells that transition to a mesenchymal phenotype lose their adherent properties and become increasingly motile. Silencing of Snail, Zeb1, Twist and other EMT associated genes correlate with a decrease in metastasis in in vivo models, and point to a critical role of EMT in metastasis [2-4]. However, analysis of tumor cells within both the primary tumor and metastatic lesions show primarily epithelial markers. Currently, it is believed that cells undergo Mesenchymal-toEpithelial Transition (MET) following their colonization into a new organ environment [5]. A recent publication by Fischer et al., used the Cre/CreER lineage-tracing genetic mouse model to explore the necessity of EMT in breast cancer metastasis [6]. Through their generation of Fibroblast Specific Protein 1 (FSP1)-GFP and Vimentin-GFP reporter mouase lines, using Cre and Cre-ER respectively, they reported that cancer cells that had not undergone EMT still metastasized just as much as those that had. The conclusions of this paper were brought into question in 2017 by Ye et al., following close scrutiny of selection of Vimentin and FSP1 promoters for the activation of EMT programs as well as the recombination efficiency of CreER [7]. We will discuss the positions held by the two contradictory publications and provide insight beyond luminal-subtype breast cancer.

Just How Critical is Epithelial-to-Mesenchymal Transition (EMT) to Metastatic Dissemination?