This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Kralova, J.
Right arrow Articles by Bose, H. R.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Kralova, J.
Right arrow Articles by Bose, H. R., Jr.

 Previous Article  |  Next Article 

Mol Cell Biol, May 1998, p. 2997-3009, Vol. 18, No. 5
0270-7306/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.

AP-1 Factors Play an Important Role in Transformation Induced by the v-rel Oncogene

Jarmila Kralova,1,2 Andrew S. Liss,1 William Bargmann,1 and Henry R. Bose Jr.1,*

Department of Microbiology and the Institute for Cellular and Molecular Biology, University of Texas at Austin, Texas 78712-1095,1 and Institute of Molecular Genetics, Czech Academy of Sciences, 166 37 Prague 6, Czech Republic2

Received 23 June 1997/Returned for modification 11 August 1997/Accepted 29 January 1998

v-rel is the oncogenic member of the Rel/NF-kappa B family of transcription factors. The mechanism by which v-Rel induces transformation of avian lymphoid cells and fibroblasts is not precisely known. However, most models propose that v-rel disrupts the normal transcriptional regulatory network. In this study we evaluated the role of AP-1 family members in v-Rel-mediated transformation. The overexpression of v-Rel, c-Rel, and c-RelDelta resulted in a prolonged elevation of c-fos and c-jun expression and in a sustained repression of fra-2 at both the mRNA and protein levels in fibroblasts and lymphoid cells. Moreover, the transforming abilities of these Rel proteins correlated with their ability to alter the expression of these AP-1 factors. v-Rel exhibited the most pronounced effect, whereas c-Rel, with poor transforming ability, elicited only moderate changes in AP-1 levels. Furthermore, c-RelDelta , which exhibits enhanced transforming potential relative to c-Rel, induced intermediate changes in AP-1 expression. To directly evaluate the role of AP-1 family members in the v-Rel transformation process, a supjun-1 transdominant mutant was used. The supjun-1 mutant functions as a general inhibitor of AP-1 activity by inhibiting AP-1-mediated transactivation and by reducing AP-1 DNA-binding activity. Coinfection or sequential infection of fibroblasts or lymphoid cells with viruses carrying rel oncogenes and supjun-1 resulted in a reduction of the transformation efficiency of the Rel proteins. The expression of supjun-1 inhibited the ability of v-Rel transformed lymphoid cells and fibroblasts to form colonies in soft agar by over 70%. Furthermore, the expression of supjun-1 strongly interfered with the ability of v-Rel to morphologically transform avian fibroblasts. This is the first report showing that v-Rel might execute its oncogenic potential through modulating the activity of early response genes.

* Corresponding author. Mailing address: Department of Microbiology, University of Texas at Austin, Austin, TX 78712-1095. Phone: (512) 471-5525. Fax: (512) 471-7088. E-mail: bose{at}mail.utexas.edu.

Mol Cell Biol, May 1998, p. 2997-3009, Vol. 18, No. 5
0270-7306/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.


This article has been cited by other articles:

  • Bolisetty, M. T., Dy, G., Tam, W., Beemon, K. L. (2009). Reticuloendotheliosis Virus Strain T Induces miR-155, Which Targets JARID2 and Promotes Cell Survival. J. Virol. 83: 12009-12017 [Abstract] [Full Text]  
  • Schnidar, H., Eberl, M., Klingler, S., Mangelberger, D., Kasper, M., Hauser-Kronberger, C., Regl, G., Kroismayr, R., Moriggl, R., Sibilia, M., Aberger, F. (2009). Epidermal Growth Factor Receptor Signaling Synergizes with Hedgehog/GLI in Oncogenic Transformation via Activation of the MEK/ERK/JUN Pathway. Cancer Res. 69: 1284-1292 [Abstract] [Full Text]  
  • Dutta, J., Fan, G., Gelinas, C. (2008). CAPER{alpha} Is a Novel Rel-TAD-Interacting Factor That Inhibits Lymphocyte Transformation by the Potent Rel/NF-{kappa}B Oncoprotein v-Rel. J. Virol. 82: 10792-10802 [Abstract] [Full Text]  
  • Gupta, N., Delrow, J., Drawid, A., Sengupta, A. M., Fan, G., Gelinas, C. (2008). Repression of B-Cell Linker (BLNK) and B-Cell Adaptor for Phosphoinositide 3-Kinase (BCAP) Is Important for Lymphocyte Transformation by Rel Proteins. Cancer Res. 68: 808-814 [Abstract] [Full Text]  
  • De Lorenzo, M. S., Yamaguchi, K., Subbaramaiah, K., Dannenberg, A. J. (2003). Bryostatin-1 Stimulates the Transcription of Cyclooxygenase-2: Evidence for an Activator Protein-1-Dependent Mechanism. Clin. Cancer Res. 9: 5036-5043 [Abstract] [Full Text]  
  • Rayet, B., Fan, Y., Gelinas, C. (2003). Mutations in the v-Rel Transactivation Domain Indicate Altered Phosphorylation and Identify a Subset of NF-{kappa}B-Regulated Cell Death Inhibitors Important for v-Rel Transforming Activity. Mol. Cell. Biol. 23: 1520-1533 [Abstract] [Full Text]  
  • Kralova, J., Liss, A. S., Bargmann, W., Pendleton, C., Varadarajan, J., Ulug, E., Bose, H. R. Jr. (2002). Differential Regulation of the Inhibitor of Apoptosis ch-IAP1 by v-rel and the Proto-Oncogene c-rel. J. Virol. 76: 11960-11970 [Abstract] [Full Text]  
  • Nehyba, J., Hrdlickova, R., Burnside, J., Bose, H. R. Jr. (2002). A Novel Interferon Regulatory Factor (IRF), IRF-10, Has a Unique Role in Immune Defense and Is Induced by the v-Rel Oncoprotein. Mol. Cell. Biol. 22: 3942-3957 [Abstract] [Full Text]  
  • Liss, A. S., Bose, H. R. Jr. (2002). Mutational Analysis of the v-Rel Dimerization Interface Reveals a Critical Role for v-Rel Homodimers in Transformation. J. Virol. 76: 4928-4939 [Abstract] [Full Text]  
  • Espinosa, L., Santos, S., Ingles-Esteve, J., Munoz-Canoves, P., Bigas, A. (2002). p65-NF{kappa}B synergizes with Notch to activate transcription by triggering cytoplasmic translocation of the nuclear receptor corepressor N-CoR. J. Cell Sci. 115: 1295-1303 [Abstract] [Full Text]  
  • Bose, H. R. Jr. (2001). Interferon Regulatory Factor 4 Contributes to Transformation of v-Rel-Expressing Fibroblasts. Mol. Cell. Biol. 21: 6369-6386 [Abstract] [Full Text]  
  • Hennigan, R. F., Stambrook, P. J. (2001). Dominant Negative c-jun Inhibits Activation of the Cyclin D1 and Cyclin E Kinase Complexes. Mol. Biol. Cell 12: 2352-2363 [Abstract] [Full Text]  
  • Yu, R., Hebbar, V., Kim, D. W., Mandlekar, S., Pezzuto, J. M., Kong, A.-N. T. (2001). Resveratrol Inhibits Phorbol Ester and UV-Induced Activator Protein 1 Activation by Interfering with Mitogen-Activated Protein Kinase Pathways. Mol. Pharmacol. 60: 217-224 [Abstract] [Full Text]  
  • Chen, C., Agnes, F., Gelinas, C. (1999). Mapping of a Serine-Rich Domain Essential for the Transcriptional, Antiapoptotic, and Transforming Activities of the v-Rel Oncoprotein. Mol. Cell. Biol. 19: 307-316 [Abstract] [Full Text]  
  • Malliri, A., Symons, M., Hennigan, R. F., Hurlstone, A. F.L., Lamb, R. F., Wheeler, T., Ozanne, B. W. (1998). The Transcription Factor AP-1 Is Required for EGF-induced Activation of Rho-like GTPases, Cytoskeletal Rearrangements, Motility, and In Vitro Invasion of A431 Cells. JCB 143: 1087-1099 [Abstract] [Full Text]  


Copyright © 2009 by the American Society for Microbiology.   For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»