✦ LIBER ✦

Selective inhibition of cyclooxygenase (COX)-2 inhibits endothelial cell proliferation by induction of cell cycle arrest

✍ Scribed by Kentaro Yazawa; Nelson H. Tsuno; Joji Kitayama; Kazushige Kawai; Yurai Okaji; Masahiro Asakage; Eiji Sunami; Shoichi Kaisaki; Nobukazu Hori; Toshiaki Watanabe; Koki Takahashi; Hirokazu Nagawa

Publisher: John Wiley and Sons
Year: 2004
Tongue: French
Weight: 336 KB
Volume: 113
Category: Article
ISSN: 0020-7136
DOI: 10.1002/ijc.20621

No coin nor oath required. For personal study only.

✦ Synopsis

High-level expression of cyclooxygenase (COX)-2 is reported in 80 -90% of colorectal adenocarcinomas. Selective inhibition of COX-2 was shown to reduce colorectal tumorigenesis in different models of carcinogenesis and to prevent metastasis in xenograft tumor models, as well as to suppress in vitro induced angiogenesis. Recently, COX-2 was reported to be expressed not only in malignant epithelial cells, but also in the neovasculature that feeds the tumor in a variety of solid human cancers. Thus, one of the possible mechanisms by which selective COX-2 inhibitor reduces tumor growth and metastasis is through inhibition of tumor angiogenesis. Although a report suggested a possible role of endothelial COX-1 in the process of angiogenesis, in a recent study, the selective inhibition of COX-2 was shown to strongly inhibit angiogenesis by inducing endothelial cell (EC) apoptosis. In the present study, using human umbilical vein endothelial cells (HUVECs) as a model of angiogenesis, we investigated the potential antiangiogenic effect of the selective COX-2 inhibitor and its mechanism of action, and clearly demonstrated that selective inhibition of COX-2 caused a dose-dependent decrease in the proliferative activity of ECs, as well as an inhibition of capillary-like tube formation. The inhibitory effect on EC proliferation was dependent on the cell cycle arrest to the G1 phase and not on cell apoptosis.

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