Neutrophil dichotomy drives lymphatic metastasis

The study provides an alternative scenario in which the response of the tumor cell population itself determines the pro-tumor versus anti-tumor outcome of neutrophil-tumor interaction. Experimentally, we show that neutrophils, which were sequentially stimulated by bacteria and tumor cell secreted factors, killed a certain proportion of tumor target cells. However, the majority of the tumor cells remained resistant to this neutrophil-mediated killing and underwent a phenotype switch that was reminiscent of partial epithelial-to-mesenchymal transition. This phenotypic switch was associated with physical escape from NK killing and resulted in enhanced lymphatic metastasis.