Reciprocally, DMBT1 knockdown in LvM16 (Supplementary Fig. S5f, g) impaired the capacity of LvM16 CM to induce CD62L+ polarization and Ccl8 expression of primary KCs (Fig. 5h, i), leading to suppressed NET formation in vitro when neutrophils were co-cultured with tumor-pretreated KCs (Fig. 5j). This evidence concerns the gene CCL8 and neoplasm.