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Originally published In Press as doi:10.1074/jbc.M208952200 on October 18, 2002

J. Biol. Chem., Vol. 277, Issue 51, 50137-50142, December 20, 2002
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Hepatocyte Growth Factor Inhibits Anoikis by Induction of Activator Protein 1-dependent Cyclooxygenase-2
IMPLICATION IN HEAD AND NECK SQUAMOUS CELL CARCINOMA PROGRESSION*

Qinghua ZengDagger §, Laurie K. McCauley, and Cun-Yu WangDagger ||

From the Dagger  Laboratory of Molecular Signaling and Apoptosis, Department of Biologic and Materials Sciences and the  Department of Periodontics, Prevention, and Geriatrics and Department of Pathology, School of Dentistry and Medicine, University of Michigan, Ann Arbor, Michigan 48109-1078

Anoikis, also called suspension-induced apoptosis, plays an important role in tumor development, progression, and metastasis. Recently we found that hepatocyte growth factor (HGF) inhibited anoikis of human head and neck squamous cell carcinoma (HNSCC) cells by activating the extracellular signal-regulated kinase (ERK)-signaling pathway. However, the anti-apoptotic effectors that were regulated by the ERK-signaling pathway were unknown. Here we report that HGF-mediated inhibition of anoikis was dependent on activator protein-1 activity through the activation of the ERK-signaling pathway. Using a combination of microarray analysis and Northern blot analysis, we found that an anti-apoptotic gene cyclooxygenase-2 (cox-2) was induced by HGF in an activator protein-1-dependent fashion. Inhibition of Cox-2 activity partially abolished HGF-mediated cell survival, and overexpression of Cox-2 in HNSCC cells provided resistance against anoikis. Moreover, HNSCC cells stably expressing Cox-2 had aggressive tumor growth in a nude mouse model compared with control cells. Taken together, our results demonstrate that Cox-2 plays an important role in HGF-mediated anoikis resistance. HGF may stimulate the progression and growth of HNSCC in vivo by induction of Cox-2.

* This work was supported by National Institutes of Health Research Grant R01-DE13848 and R01-DE13788 (to C.-Y. W.) and DK53904 (to L. K. M.).The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

§ Current address: Institute of Genetic and Cytology, School of Life Sciences, Northeast Normal University, Changchun 130021 People's Republic of China.

|| To whom correspondence should be addressed: Laboratory of Molecular Signaling and Apoptosis, Dept. Biologic and Materials Sciences, University of Michigan, 1011 N. University Ave. Ann Arbor, MI 48109-1078. Tel.: 734-615-4386; Fax: 734-764-2425; E-mail: cunywang@umich.edu.

Copyright © 2002 by The American Society for Biochemistry and Molecular Biology, Inc.
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Copyright © 2002 by the American Society for Biochemistry and Molecular Biology.