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Originally published In Press as doi:10.1074/jbc.M201598200 on May 6, 2002

J. Biol. Chem., Vol. 277, Issue 28, 25203-25208, July 12, 2002
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Hepatocyte Growth Factor Inhibits Anoikis in Head and Neck Squamous Cell Carcinoma Cells by Activation of ERK and Akt Signaling Independent of NFkappa B*

Qinghua ZengDagger §, Shaoqiong ChenDagger , Zongbing YouDagger , Fan YangDagger , Thomas E. Carey, Daniel SaimsDagger , and Cun-Yu WangDagger ||

From the Dagger  Laboratory of Molecular Signaling and Apoptosis, Department of Biologic and Materials Sciences, the  Department of Oral Pathology, Oral Medicine and Oral Oncology, University of Michigan, Ann Arbor, Michigan 48109-1078 and the § Institute of Genetic & Cytology, School of Life Sciences, Northeast Normal University, Changchun 130021, Peoples' Republic of China

Hepatocyte growth factor (HGF), also known as a scatter factor, regulates a variety of biological activities including cell proliferation, survival, migration, and angiogenesis. Importantly, HGF and its receptor c-Met have been found to be associated with metastasis of human head and neck squamous cell carcinoma (HNSCC). Because anoikis resistance plays an important role in tumor progression and metastasis, here we examined whether HGF suppressed suspension-induced apoptosis (anoikis) in HNSCC cells, and if so, we assessed downstream signaling pathways mediated by HGF. We found that HNSCC cells underwent anoikis upon loss of matrix contact, whereas HGF provided protection against it. HGF-induced anoikis resistance was found to be dependent on both ERK and Akt signaling pathways. The inhibition of either ERK or Akt activation abolished HGF-mediated survival. Furthermore, we found that HGF did not activate NFkappa B transcription in HNSCC cells and that HGF-mediated anoikis resistance was independent of NFkappa B. Taken together, our results suggest that anoikis resistance induced by HGF may also play an important role in the progression and metastasis of HNSCC.

* This work was supported by National Institutes of Health Research Grants R01-DE13848 and R01-DE13788 (to C.-Y. W.).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.

|| 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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