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Carcinogenesis Advance Access published online on February 12, 2004
Carcinogenesis, doi:10.1093/carcin/bgh110
© 2004 by Oxford University Press
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© 2004 Oxford University Press

MOLECULAR EPIDEMIOLOGY AND CANCER PREVENTION

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

Michael André Kern 1*, Mirja Mareike Schöneweiß 1, Dina Sahi 1, Maryam Bahlo 1, Anke Maria Haugg 1, Hans Udo Kasper 2, Hans Peter Dienes 1, Herbert Käferstein 3, Kai Breuhahn 1, and Peter Schirmacher 2

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

* Corresponding author. E-mail: michael.kern{at}uni-koeln-de.

Received 15 October 2003 ; revised 14 January 2004 ; accepted 3 February 2004

Abstract

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 nonspecific inhibitor (sulindac) starting 5 days prior to tumor cell injection. After 35 days mice were sacrified and tumors were analysed 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 to parental cells. Selective COX-2 inhibition led to a significant reduction of tumor growth and weight. COX-2 inhibition had a significant antiproliferative and proapoptotic 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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