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A role for FAK in the Concanavalin A-dependent secretion of matrix metalloproteinase-2 and -9

Oncogene volume 19, pages 5539–5542 (2000)Cite this article

Abstract

To study the signaling pathway critical for the secretion of matrix metalloproteinases (MMPs), we examined the role of focal adhesion kinase (FAK) in Concanavalin A (Con A)-stimulated cells. We established a cell line in which FAK gene was conditionally inducible by use of FAK-null fibroblasts and the tetracycline repression system. In this cell line, FAK expression was undetectable in the presence of tetracycline but induced within 1 day by the removal of the drug. We found that FAK expression augmented the Con A-dependent secretion of MMP-9 and MMP-2. In contrast, proteolytic activation of MMP-2 by Con A-treatment did not require FAK expression. In addition, activation of MMP-secretion and tyrosine phosphorylation of FAK by Con A, but not the proteolytic activation of MMP-2, required attachment of the cells to the extracellular matrix. Taken together, our results suggest that the FAK signaling pathway play a pivotal role in the secretion of MMPs.

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References

  • Burridge K, Turner CE and Romers LH. . 1992 J. Cell Biol. 119: 893–903.

  • Clark EA and Brugge JS. . 1995 Science 268: 233–239.

  • Hamaguchi M, Grandori C and Hanafusa H. . 1988 Mol. Cell. Biol. 8: 3053–3042.

  • Hamaguchi M, Matsuyoshi N, Ohnishi Y, Gotoh B, Takeichi M and Nagai Y. . 1993 EMBO J. 12: 307–314.

  • Hamaguchi M, Yamagata S, Thant AA, Xiao H, Iwata H, Mazaki T and Hanafusa H. . 1995 Oncogene 10: 1037–1043.

  • Hurum S, Sodek J and Aubin JE. . 1982 Biochem. Biophys. Res. Commun. 107: 357–366.

  • Ilic D, Furuta Y, Kanazawa S, Takeda N, Sobue K, Nakatsuji N, Nomura S, Fujimoto J, Okada M, Yamamoto T and Aizawa S. . 1995 Nature 377: 539–544.

  • Kataoka M, Yamagata S, Akiyama S, Watanabe T, Takagi H, Thant AA, Iida K, Saga S, Kishi J and Hamaguchi M. . 1996 Int. J. Oncol. 8: 773–779.

  • Kornberg L, Earp HS, Parson JT, Schaller M and Juliano RL. . 1992 J. Biol. Chem. 267: 23439–23442.

  • Liotta LA. . 1986 Cancer Res. 46: 1–7.

  • Overall CM and Sodek J. . 1990 J. Biol. Chem. 265: 21141–21151.

  • Shibata K, Kikkawa F, Nawa A, Nawa A, Suganuma N and Hamaguchi M. . 1997 Cancer Research 57: 5416–5420.

  • Shibata K, Kikkawa F, Nawa A, Thant AA, Naruse K, Mizutani S and Hamaguchi M. . 1998 Cancer Res. 58: 900–903.

  • Stetler-Stevenson WG, Krutzsch HC, Wacher MP, Margulies IMK and Liotta LA. . 1989 J. Biol. Chem. 264: 1353–1356.

  • Thant AA, Serbulea M, Kikkawa F, Liu E, Tomoda Y and Hamaguchi M. . 1997 FEBS Lett. 406: 28–30.

  • Thant AA, Sein TT, Liu E, Machida K, Kikkawa F, Koike T, Seiki M, Matsuda S and Hamaguchi M. . 1999 Oncogene 18: 6555–6563.

  • Weiner TM, Liu ET, Craven RJ and Cance WG. . 1993 Lancet 342: 1024–1025.

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Acknowledgements

We thank members and staff from the Hamaguchi laboratory for their technical assistance and helpful discussions. This work was supported by a Grant-in-Aid for COE research from the Ministry of Education, Science and Culture of Japan, a Grant under the Monbusho International Scientific Research Program.

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Authors and Affiliations

  1. Laboratory of Molecular Pathogenesis, Nagoya University School of Medicine, 65 Tsurumai-cho, Showa-ku, 466-8550, Nagoya, Japan

    Thet Thet Sein, Aye Aye Thant, Yukiko Hiraiwa, ARM Ruhul Amin, Yasuyoshi Sohara, Yuzhen Liu, Satoru Matsuda & Michinari Hamaguchi

  2. Department of Oncology, Institute of Medical Science, Tokyo University, 4-6-1 Shirokanedai, Minato-ku, 108-8639, Tokyo, Japan

    Tadashi Yamamoto

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  1. Thet Thet Sein
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Sein, T., Thant, A., Hiraiwa, Y. et al. A role for FAK in the Concanavalin A-dependent secretion of matrix metalloproteinase-2 and -9. Oncogene 19, 5539–5542 (2000). https://doi.org/10.1038/sj.onc.1203932

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