Figure 6

Systemic AT-MSC administration abrogates A375 tumor dormancy and AT-MSC tumor growth support can be partially blocked by inhibiting SDF-1α/CXCR4 signalling. A. Systemic administration of AT-MSC (10⁶ i.v.) concomitant with the implantation of 1 × 10⁵ A375 s.c. resulted in abrogation of tumor dormancy in 8 out of 12 cases in contrast to 1 out of 8 implantations of A375 s.c. alone. B. Cultured A375 cells or single-cell suspensions prepared by positive immunomagnetic separation of human CD44+ cells from tumor xenotransplants were stained with anti-CXCR4 antibody. Flow cytometric analysis has shown the absence of the CXCR4 marker on low density cultured A375 cells (left), CXCR4 increase upon cell confluence (middle) and high level of expression on A375 from tumor xenotransplant in vivo (right). CXCR4 (filled area), isotype control (open area). C. 2 × 10⁵ A375 were implanted s.c either alone or coimplanted with AT-MSC (10⁶ i.v.). Although all xenografts in AT-MSC injected group started to grow, animals treated with AMD3100 inhibitor of SDF-1α/CXCR4 (1.25 mg/kg every other day s.c.) exhibited significantly lower tumor volume in comparison to untreated group (*p < 0.05).