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JNCI Journal of the National Cancer Institute 2004 96(19):1473-1477; doi:10.1093/jnci/djh267
© 2004 by Oxford University Press
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© 2004 Oxford University Press

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Effects of Angiogenesis Inhibitors on Vascular Network Formation by Human Endothelial and Melanoma Cells

Daisy W. J. van der Schaft, Richard E. B. Seftor, Elisabeth A. Seftor, Angela R. Hess, Lynn M. Gruman, Dawn A. Kirschmann, Yumi Yokoyama, Arjan W. Griffioen, Mary J. C. Hendrix

Affiliations of authors: Children’s Memorial Research Center, Northwestern University Feinberg School of Medicine, Robert H. Lurie Comprehensive Cancer Center, Chicago, IL (REBS, EAS, ARH, LMG, DAK, MJCH); Angiogenesis Laboratory, Department of Pathology/Internal Medicine, Research Institute for Growth and Development (GROW), Maastricht University and Hospital, Maastricht, The Netherlands (DWJVDS, AWG); Department of Pharmacology, University of Minnesota, Minneapolis (YY)

Correspondence to: Mary J. C. Hendrix, PhD, Children’s Memorial Research Center, Northwestern University Feinberg School of Medicine, 2300 Children’s Plaza, Box 222, Chicago, IL 60614-3394 (e-mail: mjchendrix{at}childrensmemorial.org)

Endothelial cells involved in vasculogenesis and angiogenesis are key targets in cancer therapy. Recent evidence suggests that tumor cells can express some genes typically expressed by endothelial cells and form extracellular matrix–rich tubular networks, phenomena known as vasculogenic mimicry. We examined the effects of three angiogenesis inhibitors (i.e., anginex, TNP-470, and endostatin) on vasculogenic mimicry in human melanoma MUM-2B and C8161 cells and compared them with their effects in human endothelial HMEC-1 and HUVEC cells. Anginex, TNP-470, and endostatin markedly inhibited vascular cord and tube formation by HMEC-1 and HUVEC cells in vitro, whereas tubular network formation by MUM-2B and C8161 cells was relatively unaffected. Endothelial cells expressed higher mRNA and protein levels for two putative endostatin receptors, {alpha}5 integrin and heparin sulfate proteoglycan 2, than melanoma cells, suggesting a mechanistic basis for the differential response of the two cell types to angiogenesis inhibitors. These findings may contribute to the development of new antivascular therapeutic agents that target both angiogenesis and tumor cell vasculogenic mimicry.


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