Fig. 3: CXCR7 promotes melanoma proliferation through Src activation.

a The effects of CXCR7 modifications on the Src, AKT, and ERK signalings. b CXCR7 expression modulated CXCL12-stimulated Src phosphorylation in the presence of AMD3100. Murine melanoma cell lines were cultured in serum-free medium overnight. After pretreated with AMD3100 (1 μg/ml) for 1 h, the cells were stimulated with recombinant murine CXCL12 (50 ng/ml). The phosphorylation levels of Src were determined by western blot. c PP1 suppressed CXCR7-induced cell proliferation. Melanoma cells were seeded into 96-well plates in the presence of DMSO or PP1 (10 μM). After 48 h, the numbers of cells were examined by CCK-8 assays. The proliferation rates were normalized to F0 Vec cells (top) or F10 WT cells (bottom) without treatment. d Representative images and quantitative results of the clonogenic growth of cells treated with DMSO or PP1 (10 μM). The results were normalized to F0 Vec cells (top) or F10 WT cells (bottom) without treatment. e Serum-starved A375 WT and KO cells were pretreated with AMD3100 (1 μg/ml) for 1 h, and stimulated with recombinant human CXCL12 (100 ng/ml). Cells were harvested for western blot analysis of the phosphorylated Src kinase. f PP1 recapitulated the disrupted cell proliferation induced by loss of CXCR7 in A375 cells. The proliferation rates were normalized to A375 WT cells without treatment. g Clonogenic growth of A375 WT and KO cells with the same treatments described in d. The results were normalized to A375 WT cells without treatment. Proliferation experiments and colony formation assays were independently repeated three times. Data are presented as mean ± SD. **p < 0.01, ***p < 0.001