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Carcinogenesis Advance Access originally published online on February 12, 2004
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Carcinogenesis, Vol. 25, No. 7, 1193-1199, July 2004
Carcinogenesis vol.25 no.7 © Oxford University Press 2004; all rights reserved.

ARTICLE

Cyclooxygenase-2 inhibitors suppress the growth of human hepatocellular carcinoma implants in nude mice

Michael André Kern1,4, Mirja Mareike Schöneweiß1, Dina Sahi1, Maryam Bahlo1, Anke Maria Haugg1, Hans Udo Kasper1,3, Hans Peter Dienes1, Herbert Käferstein2, Kai Breuhahn1 and Peter Schirmacher1,3

1 Institute of Pathology, 2 Institute of Forensic Medicine and 3 Center for Molecular Medicine (ZMMK), University of Cologne, Joseph-Stelzmann-Str. 9, D-50931 Cologne, Germany

4 To whom correspondence should be addressed Email: michael.kern{at}uni-koeln-de

Cyclooxygenase (COX)-2 is expressed in hepatocellular carcinomas (HCCs) and HCC cell lines. COX-2 inhibition strongly suppresses growth of HCC cells in vitro by inducing apoptosis and reducing proliferation. Here, we evaluate the in vivo effects and mechanism of COX-2 inhibition of human HCC cell line derived xenotransplanted tumors in nude mice. Firstly, nude mice were treated with a COX-2 specific inhibitor (meloxicam) or a non-specific inhibitor (sulindac) starting 5 days prior to tumor cell injection. After 35 days mice were killed and tumors were analyzed morphologically and assayed for proliferation (Ki67), apoptosis (M30) and COX-2 expression. Secondly, mice were treated with meloxicam or sulindac after tumors had reached a diameter of at least 0.2 cm. COX-2 expression was maintained in implant tumors at levels comparable with parental cells. Selective COX-2 inhibition led to a significant reduction of tumor growth and weight. COX-2 inhibition had a significant anti-proliferative and pro-apoptotic effect on tumor cells. These results demonstrate that under experimental conditions selective COX-2 inhibition suppresses solid HCC growth in vivo and, therefore may have preventive and therapeutic potential for human HCCs.


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