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This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Nemoto, T. Articles by Kubota, S. Search for Related Content PubMed PubMed Citation Articles by Nemoto, T. Articles by Kubota, S. Related Collections Hemostasis, Thrombosis, and Vascular Biology Brief Reports Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  Blood, 15 February 2002, Vol. 99, No. 4, pp. 1478-1481 BRIEF REPORT Overexpression of ornithine decarboxylase enhances endothelial proliferation by suppressing endostatin expression Takahiro Nemoto, Hisae Hori, Masataka Yoshimoto, Yousuke Seyama, and Shunichiro Kubota From the Department of Physiological Chemistry and Metabolism, Graduate School of Medicine, The University of Tokyo, Japan; School of Allied Health Sciences, Faculty of Medicine, and the Department of Molecular Pathogenesis, Medical Research Institute, Tokyo Medical and Dental University, Japan; and the Department of Breast Surgery, Cancer Institute Hospital, Tokyo, Japan. Angiogenesis, an essential process for tumor growth, is regulated by endothelial proliferation factors and their inhibitors such as endostatin. Endostatin, a carboxyl-terminal fragment of type XVIII collagen, inhibits endothelial proliferation, angiogenesis, and tumor growth. Ornithine decarboxylase (ODC), a molecule that is overexpressed in various cancers, is associated with promoting tumor growth and angiogenesis. We found that ODC-overexpressing human cancer cells and breast cancer specimens showed suppressed expression of type XVIII collagen and endostatin. We hypothesized that ODC overexpression may facilitate angiogenesis in tumors by suppressing endostatin expression. ODC-overexpressing COS cells, which showed suppressed type XVIII collagen and endostatin expression, were established. Conditioned media derived from these cells, containing decreased levels of endostatin, induced significant endothelial proliferation. ODC-overexpressing cells, when transplanted into nude mice, suppressed type XVIII collagen expression and promoted neovascularization in vivo. Thus, overexpression of ODC facilitates endothelial proliferation by suppressing endostatin expression. © 2002 by The American Society of Hematology.   CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: Y. LING, N. LU, Y. GAO, Y. CHEN, S. WANG, Y. YANG, and Q. GUO Endostar Induces Apoptotic Effects in HUVECs through Activation of Caspase-3 and Decrease of Bcl-2 Anticancer Res, January 1, 2009; 29(1): 411 - 417. [Abstract] [Full Text] [PDF] C. Lopez-Garcia, A. J. Lopez-Contreras, A. Cremades, M. T. Castells, F. Marin, F. Schreiber, and R. Penafiel Molecular and Morphological Changes in Placenta and Embryo Development Associated with the Inhibition of Polyamine Synthesis during Midpregnancy in Mice Endocrinology, October 1, 2008; 149(10): 5012 - 5023. [Abstract] [Full Text] [PDF] Y. Takahashi, L. Li, M. Kamiryo, T. Asteriou, A. Moustakas, H. Yamashita, and P. Heldin Hyaluronan Fragments Induce Endothelial Cell Differentiation in a CD44- and CXCL1/GRO1-dependent Manner J. Biol. Chem., June 24, 2005; 280(25): 24195 - 24204. [Abstract] [Full Text] [PDF]

	Copyright © 2002 by American Society of Hematology         Online ISSN: 1528-0020