Journal Article

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

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

in Carcinogenesis

Volume 25, issue 7, pages 1193-1199
Published in print July 2004 | ISSN: 0143-3334
Published online July 2004 | e-ISSN: 1460-2180 | DOI:
Cyclooxygenase-2 inhibitors suppress the growth of human hepatocellular carcinoma implants in nude mice

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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.

Keywords: COX-1, COX-2, cyclooxygenase-1, -2; NSAIDs, non-steroidal anti-inflammatory drugs; HCC, hepatocellular carcinoma; PGE2, prostaglandin E2

Journal Article.  3965 words.  Illustrated.

Subjects: Clinical Cytogenetics and Molecular Genetics

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