In vivo inhibition of tumor angiogenesis by a soluble VEGFR-2 fragment

The interaction of vessel endothelial cell growth factor (VEGF) and its receptors (flt-1, FLK-1/KDR) regulates tumor angiogenesis. Therefore, blocking the binding of VEGF and the corresponding receptor has become critical for antitumor angiogenesis biological therapy. Our study extracted sFLK-1 fragment from embryo mouse liver using RT-PCR, recombined it to retrovirus vector, and transfected it to tumor cell lines (S 180 and B 16) by the liposome mediated method, then we observed the biological behavior of transgenic cells in vivo. The results are: (1) Fragment (1034 bp) was extracted from E9, E I I embryo Mouse liver tissue, which was identified by sequence analysis. (2) This fragment was cloned to retrovirus vector (PLXSN vector), which was further transfected to tumor cells lines (S 180 and B 16). SDS-PAGE indicated the Suspension of transgenic cells present sVEGFR-2(sFLK-1) fragment; Western blot identified it. (3) In Vivo Study showed that the weight and size Of tumor in the group Of transgenic cells were smaller than in control groups. Microvessel density (MVD) and FLK-1 expression were obviously different between transgenic and control groups, but there were no differences in VEGF expression between transgenic and control groups. In short, the isolated Soluble VEGFR2 fragment transfected to tumor cells can be secreted to extracellular Suspension and can inhibit turner angiogenesis in vivo. (C) 2004 Elsevier Inc. All rights reserved.