Fig. 3

CXCL8-CXCR1/2 deteriorates the malignant phenotype of GC. A Migration patterns of GC cells on Matrigel compared to cells cultured with CXCL8 and/or CXCL8-CXCR1/2 inhibitor repertaxin. B Migration trail of GC cells cultured with CXCL8 or CXCL8 and CXCL8-CXCR1/2 inhibitor. C Migration average distances of GC cells in each group. D Transwell exhibited the differences in the number of permeable cells in each group. E, F CCK-8, and colony formation assay confirmed CXCL8 could promote GC proliferation which could be inhibited by CXCL8-CXCR1/2 inhibitor. G CXCL8 increased the subcutaneous tumor size and weight. H IHC representative image of subcutaneous tumors showing that CXCL8 could promote Ki67 and inhibit the expression of Capcase3; the inhibitors could counteract this effect. I CXCL8 induced ascites formation and intra- metastasis of GC