Extended Data Fig. 3: Neutrophil-specific genetic ablation of Hilpda or Cidec did not lead to significant changes on lung metastases of breast cancer in vivo.

a–f, The neutrophil-targeting cKO mice (a-c, Hilpda-cKO; d–f, Cidec-cKO), and their wild type littermates were orthotopically implanted with AT3-g-csf cells. On day 15, the relative lipid levels in lung neutrophils were determined by BODIPY 493/503 staining and flow cytometry (a and d) (n = 5 per group), and the resected primary tumors were weighed (b and e). At the end point (day 30), spontaneous lung metastases of WT and cKO mice were quantified (c and f). n = 13 (WT group) and 14 (Hilpda-cKO group) for b, c; n = 15 (WT group) and 14 (Cidec-cKO group) for e, n = 10 (WT group) and 12 (Cidec-cKO group) for f. g, A schematic diagram showing the modified experimental lung metastasis model employed in this study. Mice were first orthotopically implanted with non-labeled AT3-g-csf cells to induce a neutrophil-high host condition. Luciferase-labeled AT3-Luc cells were then implanted intravenously on day 10, a time point within the pre-metastatic stage. On day 15, the primary tumors were resected. At the end point, the lung metastatic progression of AT3-Luc cells was detected by ex vivo BLI. h, Following the above modified experimental lung metastasis model, the lung metastatic progression of AT3-Luc cells in WT and Cidec-cKO recipient mice was determined by ex vivo BLI. Representative BLI images of the harvested lungs are shown and red lines indicate blank wells without lung tissues (left) (n = 11). n represents biologically independent animals. Data are mean ± s.e.m. and P values were determined by unpaired two-tailed t-test. ns, not significant.

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