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[Cancer Research 61, 2404-2408, March 15, 2001]
© 2001 American Association for Cancer Research

Advances in Brief

Vascular Endothelial Growth Factor (VEGF)-C Differentially Affects Tumor Vascular Function and Leukocyte Recruitment

Role of VEGF-Receptor 2 and Host VEGF-A1

Ananth Kadambi2, Carla Mouta Carreira2, Chae-ok Yun2, Timothy P. Padera, Dennis E. J. G. J. Dolmans, Peter Carmeliet, Dai Fukumura and Rakesh K. Jain3

Edwin L. Steele Laboratory, Department of Radiation Oncology, Harvard Medical School and Massachusetts General Hospital, Boston, Massachusetts 02114 [A. K., C. M. C., C-o. Y., T. P. P., D. E. J. G. J. D., D. F., R. K. J.], and The Center for Transgene Technology and Gene Therapy, KU Leuven, Leuven B-3000, Belgium [P. C.]

Unlike vascular endothelial growth factor (VEGF)-A, the effect of VEGF-C on tumor angiogenesis, vascular permeability, and leukocyte recruitment is not known. To this end, we quantified in vivo growth and vascular function in tumors derived from two VEGF-C-overexpressing (VC+) and mock-transfected cell lines (T241 fibrosarcoma and VEGF-A-/- embryonic stem cells) grown in murine dorsal skinfold chambers. VC+ tumors grew more rapidly than mock-transfected tumors and exhibited parallel increases in tumor angiogenesis. Furthermore, VEGF-C overexpression elevated vascular permeability in T241 tumors, but not in VEGF-A-/- tumors. Surprisingly, unlike VEGF-A, VEGF-C did not increase leukocyte rolling or adhesion in tumor vessels. Administration of VEGF receptor (VEGFR)-2 neutralizing antibody DC101 reduced vascular density and permeability of both VC+ and mock-transduced T241 tumors. These data suggest that VEGFR-2 signaling is critical for tumor angiogenesis and vascular permeability and that VEGFR-3 signaling does not compensate for VEGFR-2 blockade. An alternate VEGFR, VEGFR-1 or neuropilin-1, may modulate adhesion of leukocytes to tumor vessels.




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