BACKGROUND AND OBJECTIVE: Endothelial progenitor cells (EPCs) play an important role in hypoxia-triggered tumor vasculogenesis. However, the homing of exogenous EPCs in tumors is still unclear. In this study, we investigated the recruitment of exogenous EPCs in human lung adenocarcinoma model of nude mice. METHODS: EPCs labeled with green fluorescence protein (GFP) were transplanted into nude mice bearing human lung adenocarcinoma. The growth of tumor was observed. After the mice were killed, GFP-EPCs in different tissues were examined by fluorescence. The tumor tissues were stained for CD133, hypoxia-inducible factor-1alpha (HIF-1α), stromal cell-derived factor-1α (SDF-1α), and vascular endothelial growth factor receptor (KDR). Real-time polymerase chain reaction of CD133, HIF-1α, SDF-1α, and VEGF-1 were also performed. RESULTS: The growth of tumor in EPC group was significantly faster than that in saline solution group (P <0.05). Under fluorescence microscope, GFP-EPCs were strongly expressed in both tumor and bone marrow. EPCs were recruited to the tumor periphery to participate in tumor vasculogenesis. The expression of CD133, HIF-1α, and SDF-1 mRNA in tumor and bone marrow were significantly higher than that in the liver, spleen, and skin (P<0.05). CONCLUSIONS: Exogenous EPCs can be recruited to tumor and accelerate tumor growth. Except tumor, bone marrow can also recruit EPCs.
BACKGROUND AND OBJECTIVE: Endothelial progenitor cells (EPCs) play an important role in hypoxia-triggered tumor vasculogenesis. However, the homing of exogenous EPCs in tumors is still unclear. In this study, we investigated the recruitment of exogenous EPCs in humanlung adenocarcinoma model of nude mice. METHODS: EPCs labeled with green fluorescence protein (GFP) were transplanted into nude mice bearing humanlung adenocarcinoma. The growth of tumor was observed. After the mice were killed, GFP-EPCs in different tissues were examined by fluorescence. The tumor tissues were stained for CD133, hypoxia-inducible factor-1alpha (HIF-1α), stromal cell-derived factor-1α (SDF-1α), and vascular endothelial growth factor receptor (KDR). Real-time polymerase chain reaction of CD133, HIF-1α, SDF-1α, and VEGF-1 were also performed. RESULTS: The growth of tumor in EPC group was significantly faster than that in saline solution group (P <0.05). Under fluorescence microscope, GFP-EPCs were strongly expressed in both tumor and bone marrow. EPCs were recruited to the tumor periphery to participate in tumor vasculogenesis. The expression of CD133, HIF-1α, and SDF-1 mRNA in tumor and bone marrow were significantly higher than that in the liver, spleen, and skin (P<0.05). CONCLUSIONS: Exogenous EPCs can be recruited to tumor and accelerate tumor growth. Except tumor, bone marrow can also recruit EPCs.