Gene expression data from epithelial and mesenchymal tumor cells isolated from E-A14 mouse mammary tumors grown in immunodeficient and immunocompetent mice

Epithelial-mesenchymal transition (EMT) is a central oncogenic mechanism, contributing to transformation and metastatic dissemination. Several reports described that inflammation and innate immune cells favor EMT induction, contrasting with an understudied role of adaptive immunity in EMT promotion. Using an original murine mammary tumor model, we demonstrated that tumor cells maintain their epithelial phenotype in mice deficient for adaptive immune response but undergo EMT in the presence of T-cell mediated immunity. CD4 but not CD8 T cell depletion prevents EMT, undoubtedly demonstrating that CD4 T cell-mediated immunity favors EMT induction. Immune infiltrate and transcriptomic analyses revealed an inverse correlation between mesenchymal tumor cell and intratumoral neutrophil proportions, due to the reduced ability of mesenchymal cells to recruit neutrophils. Moreover, we demonstrated also the pro-EMT role of neutrophils. Last, transcriptomic database analysis of human breast tumors further strengthens the notion of a cooperation between CD4 T cells and neutrophils in EMT promotion.