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为探讨全人源抗人血管内皮生长因子受体-2(VEGFR-2)抗体Mab-04对黑素瘤的体内外抑瘤活性,分别通过流式细胞术、MTT法、细胞划痕技术和Annexin V-FITC/PI双染法检测Mab-04与不同黑素瘤细胞细胞系表面VEGFR-2的结合率、对黑素瘤细胞体外增殖能力的影响、抑制黑素瘤细胞迁移和诱导肿瘤细胞凋亡的活性。并建立B16F10小鼠黑素瘤模型,通过瘤内给药方式,给予不同剂量的抗体,使用H.E.(Hematoxylin-eosin)染色法观察Mab-04抗体的体内抗肿瘤活性。实验结果发现,Mab-04能特异性地与黑素瘤细胞表面VEGFR-2结合,有效抑制黑素瘤细胞的增殖和迁移,并能诱导黑素瘤细胞的凋亡。体内抑瘤实验也表明,Mab-04对小鼠B16F10黑素瘤模型具有明显生长抑制作用,在有效剂量范围内,抑瘤率可达到63.9%。实验表明,Mab-04能特异性地与黑素瘤细胞表面VEGFR-2受体结合,通过抑制肿瘤细胞的增殖和迁移、诱导肿瘤细胞凋亡等途径,达到抑制黑素瘤生长的作用。
To investigate the antitumor activity of human anti-human VEGFR-2 antibody Mab-04 on melanoma in vitro and in vivo, we used flow cytometry, MTT assay and cell scratch assay respectively Annexin V-FITC / PI double staining assay Mab-04 and different melanoma cell lines surface VEGFR-2 binding rate of melanoma cells in vitro proliferation, inhibit melanoma cell migration and induction of tumor cells Apoptosis activity. The B16F10 murine melanoma model was established. Anti-tumor activity of Mab-04 antibody was observed by using Hematoxylin-eosin staining in different dosages by intratumoral administration. The results showed that Mab-04 could specifically bind to VEGFR-2 on the surface of melanoma cells, effectively inhibit the proliferation and migration of melanoma cells and induce the apoptosis of melanoma cells. In vivo antitumor experiments also showed that Mab-04 had a significant growth inhibitory effect on the mouse B16F10 melanoma model, and the effective inhibition rate was 63.9%. Experiments show that Mab-04 can specifically bind to the VEGFR-2 receptor on the surface of melanoma cells and inhibit the growth of melanoma by inhibiting the proliferation and migration of tumor cells and inducing tumor cell apoptosis.