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The ability of Fos family members to produce phenotypic changes in epithelioid cells is not directly linked to their transactivation potentials

Abstract

Numerous studies have revealed distinct functions of Fos proteins in different mouse tissues and cell lines. Here, we perform a direct comparison of the features of exogenous c-Fos, Fra-1 and Fra-2 proteins expressed in murine tumor cells of epithelial origin, CSML0. Although transactivation potential of c-Fos is much stronger than that of Fra-1 and Fra-2, all three proteins are capable of modulating transcription of target genes. Moreover, there is a certain degree of specificity in the induction of the transcription of AP-1-responsive genes by different Fos proteins. For instance, c-Fos and Fra-1 but not Fra-2 activated genes of the urokinase system. Additionally, not only a strong transcriptional activator c-Fos, but also Fra-1 induced morphological alterations in CSML0 cells. N-terminal domain of Fra-1 was required for this function. On the other hand, Fra-2 failed to change morphology of CSML0 cells. We therefore conclude that c-Fos, Fra-1 and Fra-2 differently activate transcription of target genes and induce morphological changes in epithelioid carcinoma cells in a manner not directly linked to their transactivation potentials.

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References

  • Angel P, Karin M . 1991 Biochim. Biophys. Acta 1072: 129–157

  • Battista S, de Nigris F, Fedele M, Chiappetta G, Scala S, Vallone D, Pierantoni G, Megar T, Santoro M, Viglietto G, Verde P, Fusco A . 1998 Oncogene 17: 377–385

  • Bergers G, Graninger P, Braselmann S, Wrighton C, Busslinger M . 1995 Mol. Cell. Biol. 15: 3748–3758

  • Brown J, Ye H, Bronson R, Dikkes P, Greenberg M . 1996 Cell 86: 297–309

  • Chiappetta G, Tallini G, De Biasio MC, Pentimalli F, de Nigris F, Losito S, Fedele M, Battista S, Verde P, Santoro M, Fusco A . 2000 Clin. Cancer Res. 6: 4300–4307

  • Chomczynski P, Sacchi N . 1987 Analytical Biochem. 162: 156–159

  • Debinski W, Slagle-Webb B, Achen M, Stacker S, Tulchinsky E, Gillespie G, Gibo D . 2001 Mol. Med. 7: 598–608

  • Grigoriadis E, Wang Z-Q, Cecchini M, Hoffstette W, Felix R, Fleisch H, Wagner E . 1994 Science 266: 443–447

  • Jehn B, Costello E, Marti A, Keon N, Deane R, Li F, Friis R, Burry P, Martin F, Jaggi R . 1992 Mol. Cell. Biol. 12: 3890–3902

  • Jehn J, Wisdom R, Tratner I, Verma IM . 1991 Proc. Natl. Acad. Sci. USA 88: 5077–5081

  • Karin M, Liu Z-g, Zandi E . 1997 Curr. Opin. Cell. Biol. 9: 240–246

  • Kirschmeier P, Housey G, Johnson M, Perkins A, Weinstein I . 1988 DNA 7: 219–225

  • Kovary K, Bravo R . 1992 Mol. Cell. Biol. 12: 5015–5023

  • Kustikova O, Kramerov D, Grigorian M, Berezin V, Bock E, Lukanidin E, Tulchinsky E . 1998 Mol. Cell. Biol. 18: 7095–7105

  • Lepekhin EA, Walmod PS, Berezin A, Berezin V, Bock E . 2000 Methods Mol. Biol. 161: 85–100

  • Markowitz D, Goff S, Bank A . 1989 J. Virol. 62: 1120–1124

  • Matsuo K, Owens J, Tonko M, Elliot C, Chambers T, Wagner E . 2000 Nature Gen. 24: 184–187

  • Mechta F, Lallemand D, Pfarr C, Yaniv M . 1997 Oncogene 14: 837–847

  • Murakami M, Sonobe M, Ui M, Kabuyama Y, Watanabe H, Wada T, Handa H, Iba H . 1997 Oncogene 14: 2435–2444

  • Murakami M, Ui M, Iba H . 1999 Cell Growth Differ. 10: 333–342

  • Ozanne B, McGarry L, Spence H, Jonston I, Winnie J, Meagher L, Stapleton G . 2000 Eur. J. Cancer 36: 1640–1648

  • Qian X, Wang T, Rothman V, Nicosia R, Tuszynski G . 1997 Exp. Cell. Res. 235: 403–412

  • Risse-Hackl G, Adamkiewicz J, Wimmel A, Schuermann M . 1998 Oncogene 16: 3057–3068

  • Saksela K, Baltimore D . 1993 Mol. Cell. Biol. 13: 3698–3705

  • Schreiber M, Wang Z, Jochum W, Fetka I, Elliot C, Wagner E . 2000 Development 127: 4937–4948

  • Suzuki T, Okuno H, Yoshido T, Endo T, Nishina H, Iba H . 1991 Nucl. Acids Res. 19: 5537–5542

  • Tulchinsky E . 2000 Histol. Histopathol. 15: 921–928

  • Vallone D, Battista S, Pierantoni G, Fedele M, Casalino L, Santoro M, Viglietto G, Fusco A, Verde P . 1997 EMBO J. 16: 5310–5321

  • Wisdom R . 1999 Exp. Cell. Res. 253: 180–185

  • Wisdom R, Verma I . 1993 Mol. Cell. Biol. 13: 7429–7438

  • Zajchowski D, Bartholdi M, Gong Y, Webster L, Lui H, Munishkin A, Beauheim C, Harvey S, Ethier S, Johnson P . 2001 Cancer Res. 61: 5168–5178

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Acknowledgements

This work was supported by grants from Danish Cancer Society, Danish Medical Research Council and the Novo Nordisk foundation.

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Correspondence to Eugene Tulchinsky.

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Andersen, H., Mahmood, S., Tkach, V. et al. The ability of Fos family members to produce phenotypic changes in epithelioid cells is not directly linked to their transactivation potentials. Oncogene 21, 4843–4848 (2002). https://doi.org/10.1038/sj.onc.1205590

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