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[Cancer Research 62, 625-631, February 1, 2002]
© 2002 American Association for Cancer Research

Advances in Brief

Cyclooxygenase-2 Inhibition by Celecoxib Reduces Proliferation and Induces Apoptosis in Angiogenic Endothelial Cells in Vivo

Kathleen M. Leahy1, Richard L. Ornberg, Yu Wang, Ben S. Zweifel, Alane T. Koki and Jaime L. Masferrer

Pharmacia, Chesterfield, Missouri 63017

Cyclooxygenase-2 (COX-2) is expressed within neovascular structures that support many human cancers. Inhibition of COX-2 by celecoxib delays tumor growth and metastasis in xenograft tumor models as well as suppresses basic fibroblast growth factor 2 (FGF-2)-induced neovascularization of the rodent cornea. The present studies were undertaken to evaluate possible mechanisms of the antiangiogenic and anticancer effects of celecoxib. Prostaglandin E2 (PGE2) and thromboxane B2 (TXB2) were increased in rat corneas implanted with slow-release pellets containing FGF-2 (338.6 ng of PGE2/g and 17.53 ng of TXB2/g) compared with normal rat corneas (63.1 ng of PGE2/g and 2.0 ng of TXB2/g). Celecoxib at 30 mg/kg/day p.o. inhibited angiogenesis (78.6%) and prostaglandin production by 78% for PGE2 (72.65 ng/g) and 68% for TXB2 (5.55 ng/g). Decreased prostaglandin production in corneas was associated with a 2.5-fold cellular increase in apoptosis and a 65% decrease in proliferation. Similar reductions in proliferation were observed in neovascular stroma (65–70%) of celecoxib-treated (dietary 160 ppm/day) xenograft tumors as well as in tumor cells (50–75%). Apoptosis was also increased in the tumor cells (2.2–3.0-fold) in response to celecoxib. Thus, the antitumor activity of celecoxib may be attributable, at least in part, to a direct effect on host stromal elements, such as the angiogenic vasculature.




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