Ortéga N, Jonca F, Vincent S, Favard C, Malavaud B, Bertrand N, Mazerolles C, Richmann P, Pouliquen Y, Sarrammon J P, Ruchoux M M, Plouët J
Laboratoire de biologie moléculaire eucaryote, CNRS UPR 9006, Toulouse, France.
C R Acad Sci III. 1996 May;319(5):411-5.
We took advantage of the anti-idiotypic strategy to design circulating probes mimicking the biological effects of VEGF (vascular endothelial growth factor) or FGF2 (fibroblast growth factor 2). The activation of the VEGF receptor KDR/flk-1 induced endothelial cell proliferation but not their migration, whereas that of the FGF receptor FGF-R1 gave opposite results. The long lasting delivery of KDR/flk-1 agonists, but not that of FGF-R1, in nude mice grafted with tumor fragments enhanced the tumor volume. Microscopic examination showed an increase in both the vascularization and the proliferation of cancer cells. In contrast, no difference in cell proliferation was observed within normal tissues.
我们利用抗独特型策略设计了模拟血管内皮生长因子(VEGF)或成纤维细胞生长因子2(FGF2)生物学效应的循环探针。VEGF受体KDR/flk-1的激活可诱导内皮细胞增殖,但不会诱导其迁移,而FGF受体FGF-R1的激活则产生相反的结果。在接种肿瘤片段的裸鼠中,长期递送KDR/flk-1激动剂可增加肿瘤体积,而递送FGF-R1激动剂则无此效果。显微镜检查显示血管生成和癌细胞增殖均增加。相比之下,正常组织内未观察到细胞增殖的差异。