| Objective: To observe the effects of AMD3100, a blocker of SDF-1/CXCR4axis, and co-treat with Endostar on tumor angiogenesis and pulmonary metastasis inBALB/c4T1mouse breast cancer model.Method: BALB/c4T1mouse is breast cancer model was established, theywere randomly divided into four groups: control group (n=6, NS20mL/Kg),Endostar group (n=6, Endostar10mg/kg), AMD3100group (n=6, AMD31002.5mg/kg), Endostar+AMD3100group(n=6, Endostar10mg/kg and AMD3100,2.5mg/kg), all medicine were given intraperitoneal injection, once a day for2weeks.Then the weight and size of tumors were measured, the effect of inhibiting tumorgrowth treat with AMD3100and co-treat with Endostar in the mouse were observed.And the transplanted tumor microvascular density(MVD) was observed, theexpression of tumor tissue VEGF protein and mRNA was detected byimmunohistochemical an RT-PCR, the lung tissue was taken out, the metastasisnodules number of lung surface was observed by anatomical microscope and HEstaining was observed, the reduction rate of transfer nodules was calculated.Result: MVD value of control group, AMD3100group, Endostar group,AMD3100+Endostar group was (30.0±3.0),(18.1±2.7),(16.9±3.1),(10.3±2.8)respectively. Compared with control, AMD3100group could significantly suppresstumor MVD (p <0.01); combined treatment group that tumor MVD was obviouslylower than AMD3100and Endostar singe-agent group (p<0.01). Immunochemicalshowed that the expression rate of VEGF protein in transplant tumor of AMD3100group were16.33%, compared with the control group was83.67%, there wassignificant difference(p <0.05); RT-PCR showed the grey level of VEGF mRNA oftransplant tumor in AMD3100group was obviously lower than the control group by56.76%, a significant difference(p <0.01). The weight of control group,AMD3100 group, Endostar group, and AMD3100+Endostar group was (2.87±0.37),(2.02±0.4),(1.93±0.38),(1.26±0.25)g, respectively. Compared with the control,AMD3100group had a significant difference (P <0.05), joint group weight wassignificantly lower than the AMD3100and Endostar group (P <0.05). AMD3100group lung metastases nodules of the surface was (3.2±2.6), it was much lower thanthe control group (13.0±3.9)(P <0.01).Conclusion:1.The AMD3100, a blocker of SDF-1/CXCR4axis, could significantly inhibitthe tumor angiogenesis and pulmonary metastasis.2. Co-treated with SDF-1/CXCR4axis blockers AMD3100and recombinanthuman endostatin have could enhance the effect of suppress tumor angiogenesis.3. The AMD3100, a blocker of SDF-1/CXCR4axis could be inhibit the tumorangiogenesis by down-regulation the expression of VEGF. |
PDF Full Text Request