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ENGLISH ABSTRACT
JOURNAL ARTICLE
RESEARCH SUPPORT, NON-U.S. GOV'T
[Effect of vascular endothelial growth factor-C on the cell growth and angiogenesis in NB4 cell xenograft tumor].
Zhonghua Xue Ye Xue za Zhi = Zhonghua Xueyexue Zazhi 2011 Februrary
OBJECTIVE: To establish NB4/VEGF-C cells xenograft in nude mice model, and explore the effect of VEGF-C on hematological malignancies
METHODS: NB4/VEGF-C or NB4/pcDNA3.1 cell lines were established by transfecting the recombinant pcDNA3.1-VEGF-C plasmid and the vacant pcDNA3.1 vector into NB4 cells. The recombinant VEGF-C was identified by RT-PCR and Western blotting. Eighteen male BALB/c nude mice aged 4 - 5 weeks were equally divided into two groups. Mice irradiated by 4 Gy ⁶⁰Co were subcutaneously injected with 1 × 10⁷NB4/VEGF-C or NB4/pcDNA3.1 cells into one side of axilla. The volumes of xenograft tumor was evaluated according to L × t² × 0.52. Microvessel density (MVD) on the xenograft tumor section was detected by IHC with VWF antibody.
RESULTS: NB4 cell xenograft tumors were developed in all mice of both the two groups. The growth of NB4/VEGF-C cells in nude mice was faster than in controls. There were statistically significant differences in the volume and weight of xenograft tumor between NB4/VEGF-C and NB4/pcDNA3.1 cell groups [(631.44 ± 114.42) mm³ vs (491.22 ± 70.05) mm³] (P = 0.006) and [(321.78 ± 27.84) mg vs (288.57 ± 40.12) mg] (P = 0.031), respectively. MVD in xenograft tumor of NB4/VEGF-C cells [(50.8 ± 11.7)/mm²] was higher than that in controls [(18.9 ± 7.0)/mm²] (P = 0.021). The Bcl-2 protein level in NB4/VEGF-C cells xenografts was higher than that in controls.
CONCLUSION: VEGF-C could promote proliferation of NB4 cells by inducing angiogenesis and inhibit cells apoptosis by upregulating antiapoptotic Bcl-2 protein expression in NB4 cells xenograft tumor.
METHODS: NB4/VEGF-C or NB4/pcDNA3.1 cell lines were established by transfecting the recombinant pcDNA3.1-VEGF-C plasmid and the vacant pcDNA3.1 vector into NB4 cells. The recombinant VEGF-C was identified by RT-PCR and Western blotting. Eighteen male BALB/c nude mice aged 4 - 5 weeks were equally divided into two groups. Mice irradiated by 4 Gy ⁶⁰Co were subcutaneously injected with 1 × 10⁷NB4/VEGF-C or NB4/pcDNA3.1 cells into one side of axilla. The volumes of xenograft tumor was evaluated according to L × t² × 0.52. Microvessel density (MVD) on the xenograft tumor section was detected by IHC with VWF antibody.
RESULTS: NB4 cell xenograft tumors were developed in all mice of both the two groups. The growth of NB4/VEGF-C cells in nude mice was faster than in controls. There were statistically significant differences in the volume and weight of xenograft tumor between NB4/VEGF-C and NB4/pcDNA3.1 cell groups [(631.44 ± 114.42) mm³ vs (491.22 ± 70.05) mm³] (P = 0.006) and [(321.78 ± 27.84) mg vs (288.57 ± 40.12) mg] (P = 0.031), respectively. MVD in xenograft tumor of NB4/VEGF-C cells [(50.8 ± 11.7)/mm²] was higher than that in controls [(18.9 ± 7.0)/mm²] (P = 0.021). The Bcl-2 protein level in NB4/VEGF-C cells xenografts was higher than that in controls.
CONCLUSION: VEGF-C could promote proliferation of NB4 cells by inducing angiogenesis and inhibit cells apoptosis by upregulating antiapoptotic Bcl-2 protein expression in NB4 cells xenograft tumor.
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