Abstract
We investigated the attachment and spreading of v-Crk-transformed cells, v-Crk3Y1, on fibronectin. Transformation by v-Crk virtually suppressed the spreading, but not the attachment, of cells on fibronectin. This suppression of cell spreading was not correlated with the suppression of integrin α5 and β1 expression. However, the spreading of v-Crk3Y1 on fibronectin was dramatically restored by either expression of dominant-negative Ras or treatment with manumycin A, a Ras farnesyltransferase inhibitor. Moreover, both expression of dominant-negative MEK1 and treatment of cells with U0126, a MEK1 inhibitor, restored the cell spreading of v-Crk3Y1. In contrast, neither treatment with LY294002, a PI3K inhibitor, nor expression of dominant-negative C3G showed no effect on cell spreading on fibronectin. Taken together, our results suggest that, among multiple signaling pathways activated by v-Crk, the Ras-MEK1-MAP kinase cascade plays a pivotal role in the suppression of cell spreading on fibronectin, but C3G and the PI3 kinase do not.
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References
Adams SL, Sobel ME, Howard BH, Olden K, Yamada KM, Pastan I, de Crombrugghe B . 1977 Proc. Natl. Acad. Sci. USA 73: 3399–3403
Akagi T, Shishido T, Murata K, Hanafusa H . 2000 Proc. Natl. Acad. Sci. USA 97: 7290–7295
Birge RB, Knudson BS, Besser D, Hanafusa H . 1996 Genes Cells 1: 595–613
Campbell SL, Khosravi-Far R, Rossman KL, Clark GJ, Der CJ . 1998 Oncogene 17: 1395–1413
Clark EA, Brugge JS . 1995 Science 268: 233–239
Egan SE, Weinberg RA . 1993 Nature 365: 781–783
Feig AL, Cooper MG . 1988 Mol. Cel. Biol. 8: 3235–3243
Fincham VJ, James M, Frame MC, Winder SJ . 2000 EMBO J. 19: 2911–2923
Greulich H, Hanafusa H . 1996 Cell Growth Differ. 7: 1443–1451
Guan JL, Shalloway D . 1992 Nature 358: 690–692
Hynes RO . 1992 Cell 69: 11–25
Ilic D, Furuta Y, Kanazawa S, Takeda N, Sobue K, Nakatsuji N, Nomura S, Fujimoto J, Okada M, Yamamoto T . 1995 Nature 377: 539–544
Kurata H, Thant AA, Matsuo S, Senga T, Okazaki K, Hotta N, Hamaguchi M . 2000 Exp. Cell Res. 254: 180–188
Liu E, Thant AA, Kikkawa F, Kurata H, Tanaka S, Nawa A, Mizutani S, Matsuda S, Hanafusa H, Hamaguchi M . 2000 Cancer Res. 60: 2361–2364
Liu F, Sells MA, Chernoff J . 1998 Mol. Cell. Biol. 18: 250–259
Mayer BJ, Hamaguchi M, Hanafusa H . 1988 Nature 332: 272–275
Miyamoto S, Akiyama SK, Yamada KM . 1995 Science 267: 883–885
Nigg EA, Sefton BM, Singer SJ, Vogt PK . 1986 Virology 151: 50–65
Olden K, Yamada KM . 1977 Cell 11: 957–969
Plantefaber LC, Hynes RO . 1989 Cell 56: 281–290
Tanaka S, Ouchi T, Hanafusa H . 1997 Proc. Natl. Acad. Sci. USA 94: 2356–2361
Acknowledgements
We thank members of the Hamaguchi laboratory for their helpful discussions, and Mary Dutta for correction of English. This work was supported by a Grant-in-Aid for COE research from the Ministry of Education, Science and Culture of Japan.
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Liu, Y., Hiraiwa, Y., Liu, E. et al. Suppression of cell spreading by v-Crk requires Ras-MEK-MAP kinase signaling. Oncogene 20, 5908–5912 (2001). https://doi.org/10.1038/sj.onc.1204738
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DOI: https://doi.org/10.1038/sj.onc.1204738
