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[Cancer Research 60, 4596-4601, August 15, 2000]
© 2000 American Association for Cancer Research

Tumor Biology

The N-myc Oncogene in Human Neuroblastoma Cells: Down-Regulation of an Angiogenesis Inhibitor Identified as Activin A1

Stephen Breit, Keith Ashman, Jörg Wilting, Jochen Rössler, Elissavet Hatzi, Theodore Fotsis2 and Lothar Schweigerer2,3

Abteilung Hämatologie, Onkologie und Endokrinologie, Universitäts-Kinderklinik Essen, 45122 Essen, Germany [S. B., J. R., L. S.]; Protein and Peptide Group, European Molecular Biology Laboratory, 69117 Heidelberg, Germany [K. A.]; Anatomisches Institut II, Albert-Ludwigs-Universität Freiburg, 79104 Freiburg, Germany [J. W.]; and Laboratory of Biological Chemistry, University of Ioannina, 45110 Ioannina, Greece [E. H., T. F.]

Angiogenesis, the formation of new blood vessels, is seen during embryonic development and tumor progression, but the mechanisms have remained unclear. Recent data indicate that developmental and tumor angiogenesis can be induced by cellular oncogenes, leading to the enhanced activity of molecules stimulating angiogenesis. However, activated oncogenes might also facilitate angiogenesis by down-regulating endogenous inhibitors of angiogenesis. We report here that enhanced expression of the N-myc oncogene in human neuroblastoma cells down-regulates an inhibitor of endothelial cell proliferation, identified by amino acid sequencing as being identical with activin A, a developmentally regulated protein. Down-regulation appears to involve interaction of the N-Myc protein with the activin A promoter. In addition, activin A inhibits both endothelial cell proliferation in vitro and angiogenesis in vivo, and it induces hemorrhage in vivo. We suggest that the N-myc-induced down-regulation of activin A could contribute to developmental and tumor angiogenesis.




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