Cyclooxygenase regulates angiogenesis induced by colon cancer cells.

Authors: Tsujii, M  Kawano, S  Tsuji, S  Sawaoka, H  Hori, M  DuBois, RN 
Citation: Tsujii M, etal., Cell. 1998 May 29;93(5):705-16.
Pubmed: (View Article at PubMed) PMID:9630216

To explore the role of cyclooxygenase (COX) in endothelial cell migration and angiogenesis, we have used two in vitro model systems involving coculture of endothelial cells with colon carcinoma cells. COX-2-overexpressing cells produce prostaglandins, proangiogenic factors, and stimulate both endothelial migration and tube formation, while control cells have little activity. The effect is inhibited by antibodies to combinations of angiogenic factors, by NS-398 (a selective COX-2 inhibitor), and by aspirin. NS-398 does not inhibit production of angiogenic factors or angiogenesis induced by COX-2-negative cells. Treatment of endothelial cells with aspirin or a COX-1 antisense oligonucleotide inhibits COX-1 activity/expression and suppresses tube formation. Cyclooxygenase regulates colon carcinoma-induced angiogenesis by two mechanisms: COX-2 can modulate production of angiogenic factors by colon cancer cells, while COX-1 regulates angiogenesis in endothelial cells.

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CRRD Object Information
CRRD ID: 5135054
Created: 2011-07-12
Species: All species
Last Modified: 2011-07-12
Status: ACTIVE



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RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.